Subjects -> ENVIRONMENTAL STUDIES (Total: 960 journals)
    - ENVIRONMENTAL STUDIES (853 journals)
    - POLLUTION (31 journals)
    - TOXICOLOGY AND ENVIRONMENTAL SAFETY (58 journals)
    - WASTE MANAGEMENT (18 journals)

ENVIRONMENTAL STUDIES (853 journals)                  1 2 3 4 5 | Last

Showing 1 - 200 of 378 Journals sorted alphabetically
ACS Chemical Health & Safety     Hybrid Journal   (Followers: 5)
ACS ES&T Engineering     Hybrid Journal   (Followers: 9)
Acta Brasiliensis     Open Access   (Followers: 3)
Acta Ecologica Sinica     Open Access   (Followers: 11)
Acta Environmentalica Universitatis Comenianae     Open Access   (Followers: 1)
Acta Limnologica Brasiliensia     Open Access   (Followers: 4)
Acta Oecologica     Hybrid Journal   (Followers: 12)
Acta Regionalia et Environmentalica     Open Access   (Followers: 1)
Advanced Electronic Materials     Hybrid Journal   (Followers: 7)
Advanced Energy and Sustainability Research     Open Access   (Followers: 8)
Advanced Sustainable Systems     Hybrid Journal   (Followers: 8)
Advances in Ecological Research     Full-text available via subscription   (Followers: 45)
Advances in Environmental Chemistry     Open Access   (Followers: 11)
Advances in Environmental Sciences - International Journal of the Bioflux Society     Open Access   (Followers: 21)
Advances in Environmental Technology     Open Access   (Followers: 1)
Advances in Life Science and Technology     Open Access   (Followers: 23)
Advances in Tropical Biodiversity and Environmental Sciences     Open Access   (Followers: 5)
Aeolian Research     Hybrid Journal   (Followers: 6)
African Journal of Environmental Science and Technology     Open Access   (Followers: 5)
Agricultura Tecnica     Open Access   (Followers: 5)
Agricultural & Environmental Letters     Open Access   (Followers: 3)
Agro-Science     Full-text available via subscription   (Followers: 3)
Agroecological journal     Open Access  
Agronomy for Sustainable Development     Open Access   (Followers: 22)
Agrosystems, Geosciences & Environment     Open Access   (Followers: 7)
Amazon's Research and Environmental Law     Open Access   (Followers: 5)
Ambiência     Open Access  
Ambiens. Revista Iberoamericana Universitaria en Ambiente, Sociedad y Sustentabilidad     Open Access   (Followers: 1)
Ambiente & sociedade     Open Access   (Followers: 3)
Ambiente & Agua : An Interdisciplinary Journal of Applied Science     Open Access   (Followers: 1)
American Journal of Energy and Environment     Open Access   (Followers: 5)
American Journal of Environmental Engineering     Open Access   (Followers: 16)
American Journal of Environmental Protection     Open Access   (Followers: 9)
American Journal of Environmental Sciences     Open Access   (Followers: 11)
American Naturalist     Full-text available via subscription   (Followers: 85)
Annals of Civil and Environmental Engineering     Open Access   (Followers: 3)
Annals of Environmental Science and Toxicology     Open Access   (Followers: 3)
Annals of GIS     Open Access   (Followers: 29)
Annual Review of Ecology, Evolution, and Systematics     Full-text available via subscription   (Followers: 89)
Annual Review of Environment and Resources     Full-text available via subscription   (Followers: 16)
Annual Review of Pharmacology and Toxicology     Full-text available via subscription   (Followers: 36)
Annual Review of Resource Economics     Full-text available via subscription   (Followers: 10)
Applied and Environmental Soil Science     Open Access   (Followers: 20)
Applied Ecology and Environmental Sciences     Open Access   (Followers: 30)
Applied Environmental Education & Communication     Hybrid Journal   (Followers: 19)
Applied Journal of Environmental Engineering Science     Open Access   (Followers: 2)
Aquatic Ecology     Hybrid Journal   (Followers: 39)
Aquatic Toxicology     Hybrid Journal   (Followers: 25)
Arcada : Revista de conservación del patrimonio cultural     Open Access   (Followers: 2)
Architecture, Civil Engineering, Environment     Open Access   (Followers: 4)
Archives des Maladies Professionnelles et de l'Environnement     Full-text available via subscription  
Archives of Environmental and Occupational Health     Hybrid Journal   (Followers: 12)
Archives of Environmental Contamination and Toxicology     Hybrid Journal   (Followers: 14)
Archives of Toxicology     Hybrid Journal   (Followers: 20)
Arctic Environmental Research     Open Access   (Followers: 1)
Asian Journal of Environment & Ecology     Open Access   (Followers: 1)
Asian Journal of Rural Development     Open Access   (Followers: 9)
Asian Review of Environmental and Earth Sciences     Open Access   (Followers: 3)
ATBU Journal of Environmental Technology     Open Access   (Followers: 5)
Atmospheric and Climate Sciences     Open Access   (Followers: 35)
Atmospheric Environment     Hybrid Journal   (Followers: 75)
Atmospheric Environment : X     Open Access   (Followers: 3)
Augm Domus : Revista electrónica del Comité de Medio Ambiente de AUGM     Open Access  
Austral Ecology     Hybrid Journal   (Followers: 18)
Australasian Journal of Environmental Management     Hybrid Journal   (Followers: 13)
Australasian Journal of Human Security     Full-text available via subscription   (Followers: 1)
Australian Journal of Environmental Education     Full-text available via subscription   (Followers: 11)
Basic & Clinical Pharmacology & Toxicology     Hybrid Journal   (Followers: 13)
Basic and Applied Ecology     Hybrid Journal   (Followers: 25)
Behavioral Ecology     Hybrid Journal   (Followers: 60)
Behavioral Ecology and Sociobiology     Hybrid Journal   (Followers: 38)
Biocenosis     Open Access  
Biochar     Hybrid Journal   (Followers: 3)
Biodegradation     Hybrid Journal   (Followers: 2)
Biodiversity     Hybrid Journal   (Followers: 30)
Biofouling: The Journal of Bioadhesion and Biofilm Research     Hybrid Journal   (Followers: 7)
Bioremediation Journal     Hybrid Journal   (Followers: 5)
BioRisk     Open Access   (Followers: 3)
BMC Ecology     Open Access   (Followers: 24)
Boletín Instituto de Derecho Ambiental y de los Recursos Naturales     Open Access  
Boletín Semillas Ambientales     Open Access  
Boston College Environmental Affairs Law Review     Open Access   (Followers: 7)
Bothalia : African Biodiversity & Conservation     Open Access   (Followers: 1)
Built Environment     Full-text available via subscription   (Followers: 5)
Bulletin of Environmental Contamination and Toxicology     Hybrid Journal   (Followers: 15)
Bulletin of the American Meteorological Society     Open Access   (Followers: 51)
Bumi Lestari Journal of Environment     Open Access  
Canadian Journal of Earth Sciences     Hybrid Journal   (Followers: 23)
Canadian Journal of Remote Sensing     Full-text available via subscription   (Followers: 50)
Canadian Journal of Soil Science     Full-text available via subscription   (Followers: 14)
Canadian Water Resources Journal     Hybrid Journal   (Followers: 20)
Capitalism Nature Socialism     Hybrid Journal   (Followers: 27)
Carbon Resources Conversion     Open Access   (Followers: 3)
Case Studies in Chemical and Environmental Engineering     Open Access   (Followers: 1)
Casopis Slezskeho Zemskeho Muzea - serie A - vedy prirodni     Open Access  
Cell Biology and Toxicology     Hybrid Journal   (Followers: 12)
Chain Reaction     Full-text available via subscription  
Challenges in Sustainability     Open Access   (Followers: 12)
Chemical Research in Toxicology     Hybrid Journal   (Followers: 25)
Chemico-Biological Interactions     Hybrid Journal   (Followers: 3)
Chemosphere     Hybrid Journal   (Followers: 17)
Child and Adolescent Mental Health     Hybrid Journal   (Followers: 71)
China Population, Resources and Environment     Full-text available via subscription   (Followers: 4)
Ciencia, Ambiente y Clima     Open Access   (Followers: 3)
City and Environment Interactions     Open Access   (Followers: 4)
Civil and Environmental Engineering     Open Access   (Followers: 8)
Civil and Environmental Engineering Reports     Open Access   (Followers: 9)
Civil and Environmental Research     Open Access   (Followers: 22)
CLEAN - Soil, Air, Water     Hybrid Journal   (Followers: 21)
Clean Technologies     Open Access   (Followers: 1)
Clean Technologies and Environmental Policy     Hybrid Journal   (Followers: 5)
Cleanroom Technology     Full-text available via subscription   (Followers: 1)
Climate and Energy     Full-text available via subscription   (Followers: 7)
Climate Change Ecology     Open Access  
Climate Change Economics     Hybrid Journal   (Followers: 33)
Climate Policy     Hybrid Journal   (Followers: 51)
Climate Resilience and Sustainability     Open Access   (Followers: 21)
Coastal Engineering Journal     Hybrid Journal   (Followers: 9)
Cogent Environmental Science     Open Access  
Columbia Journal of Environmental Law     Open Access   (Followers: 15)
Computational Ecology and Software     Open Access   (Followers: 11)
Computational Water, Energy, and Environmental Engineering     Open Access   (Followers: 5)
Conservation and Society     Open Access   (Followers: 14)
Conservation Letters     Open Access   (Followers: 51)
Conservation Science     Open Access   (Followers: 30)
Consilience : The Journal of Sustainable Development     Open Access   (Followers: 3)
Contemporary Problems of Ecology     Hybrid Journal   (Followers: 4)
Critical Reviews in Environmental Science and Technology     Hybrid Journal   (Followers: 15)
Critical Reviews in Toxicology     Hybrid Journal   (Followers: 26)
Cuadernos de Investigación Geográfica / Geographical Research Letters     Open Access  
Culture, Agriculture, Food and Environment     Hybrid Journal   (Followers: 26)
Culture, Agriculture, Food and Environment     Hybrid Journal   (Followers: 11)
Current Environmental Engineering     Hybrid Journal  
Current Environmental Health Reports     Hybrid Journal   (Followers: 2)
Current Forestry Reports     Hybrid Journal   (Followers: 1)
Current Landscape Ecology Reports     Hybrid Journal   (Followers: 2)
Current Opinion in Environmental Science & Health     Hybrid Journal   (Followers: 1)
Current Opinion in Environmental Sustainability     Hybrid Journal   (Followers: 17)
Current Research in Ecological and Social Psychology     Open Access  
Current Research in Environmental Sustainability     Open Access   (Followers: 2)
Current Research in Green and Sustainable Chemistry     Open Access   (Followers: 1)
Current Research in Microbiology     Open Access   (Followers: 27)
Current Sustainable/Renewable Energy Reports     Hybrid Journal   (Followers: 9)
Current World Environment     Open Access   (Followers: 7)
Developments in Atmospheric Science     Full-text available via subscription   (Followers: 31)
Developments in Earth and Environmental Sciences     Full-text available via subscription   (Followers: 3)
Developments in Earth Surface Processes     Full-text available via subscription   (Followers: 1)
Developments in Environmental Modelling     Full-text available via subscription   (Followers: 8)
Developments in Environmental Science     Full-text available via subscription   (Followers: 4)
Developments in Integrated Environmental Assessment     Full-text available via subscription   (Followers: 5)
Die Bodenkultur : Journal of Land Management, Food and Environment     Open Access   (Followers: 2)
Disaster Prevention and Management     Hybrid Journal   (Followers: 32)
Discover Sustainability     Open Access   (Followers: 3)
disP - The Planning Review     Hybrid Journal   (Followers: 1)
Divulgación Científica     Open Access   (Followers: 1)
Drug and Chemical Toxicology     Hybrid Journal   (Followers: 16)
Duke Environmental Law & Policy Forum     Open Access   (Followers: 7)
Dynamiques Environnementales     Open Access   (Followers: 1)
E3S Web of Conferences     Open Access   (Followers: 2)
Earth and Environmental Science Transactions of the Royal Society of Edinburgh     Hybrid Journal   (Followers: 6)
Earth Interactions     Open Access   (Followers: 13)
Earth Science Informatics     Hybrid Journal   (Followers: 5)
Earth System Governance     Open Access  
Earth System Science Data (ESSD)     Open Access   (Followers: 8)
Earth Systems and Environment     Hybrid Journal   (Followers: 3)
Earthquake Science     Hybrid Journal   (Followers: 14)
EchoGéo     Open Access  
Eco-Thinking     Open Access   (Followers: 5)
Ecocycles     Open Access   (Followers: 6)
Ecohydrology     Hybrid Journal   (Followers: 11)
Ecohydrology & Hydrobiology     Full-text available via subscription   (Followers: 4)
Ecologia Aplicada     Open Access  
Ecología en Bolivia     Open Access  
Ecological Applications     Full-text available via subscription   (Followers: 213)
Ecological Chemistry and Engineering S     Open Access   (Followers: 4)
Ecological Complexity     Hybrid Journal   (Followers: 7)
Ecological Engineering     Hybrid Journal   (Followers: 4)
Ecological Engineering : X     Open Access  
Ecological Indicators     Hybrid Journal   (Followers: 23)
Ecological Informatics     Hybrid Journal   (Followers: 4)
Ecological Management & Restoration     Hybrid Journal   (Followers: 15)
Ecological Modelling     Hybrid Journal   (Followers: 96)
Ecological Monographs     Full-text available via subscription   (Followers: 39)
Ecological Processes     Open Access   (Followers: 2)
Ecological Questions     Open Access   (Followers: 4)
Ecological Research     Hybrid Journal   (Followers: 12)
Ecological Restoration     Full-text available via subscription   (Followers: 23)
Ecologist, The     Full-text available via subscription   (Followers: 23)
Ecology     Full-text available via subscription   (Followers: 482)
Ecology and Evolution     Open Access   (Followers: 104)
Ecology Letters     Hybrid Journal   (Followers: 341)
EcoMat : Functional Materials for Green Energy and Environment     Open Access   (Followers: 3)
Economics and Policy of Energy and the Environment     Full-text available via subscription   (Followers: 14)
Économie rurale     Open Access   (Followers: 3)
Ecoprint : An International Journal of Ecology     Open Access   (Followers: 6)
Ecopsychology     Hybrid Journal   (Followers: 8)
Ecosphere     Open Access   (Followers: 9)
Ecosystem Services     Hybrid Journal   (Followers: 10)
Ecosystems     Hybrid Journal   (Followers: 33)
Ecosystems and People     Open Access   (Followers: 3)

        1 2 3 4 5 | Last

Similar Journals
Journal Cover
Cell Biology and Toxicology
Journal Prestige (SJR): 0.924
Citation Impact (citeScore): 5
Number of Followers: 12  
 
  Hybrid Journal Hybrid journal (It can contain Open Access articles)
ISSN (Print) 1573-6822 - ISSN (Online) 0742-2091
Published by Springer-Verlag Homepage  [2658 journals]
  • Mitochondrial dynamics regulators: implications for therapeutic
           intervention in cancer

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      Abstract: Regardless of the recent advances in therapeutic developments, cancer is still among the primary causes of death globally, indicating the need for alternative therapeutic strategies. Mitochondria, a dynamic organelle, continuously undergo the fusion and fission processes to meet cell requirements. The balanced fission and fusion processes, referred to as mitochondrial dynamics, coordinate mitochondrial shape, size, number, energy metabolism, cell cycle, mitophagy, and apoptosis. An imbalance between these opposing events alters mitochondWangrial dynamics, affects the overall mitochondrial shape, and deregulates mitochondrial function. Emerging evidence indicates that alteration of mitochondrial dynamics contributes to various aspects of tumorigenesis and cancer progression. Therefore, targeting the mitochondrial dynamics regulator could be a potential therapeutic approach for cancer treatment. This review will address the role of imbalanced mitochondrial dynamics in mitochondrial dysfunction during cancer progression. We will outline the clinical significance of mitochondrial dynamics regulators in various cancer types with recent updates in cancer stemness and chemoresistance and its therapeutic potential and clinical utility as a predictive biomarker. Graphical abstract
      PubDate: 2021-10-18
       
  • Development, scrutiny, and modulation of transient reporter gene assays of
           the xenobiotic metabolism pathway in zebrafish hepatocytes

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      Abstract: The “toxicology in the twenty-first century” paradigm shift demands the development of alternative in vitro test systems. Especially in the field of ecotoxicology, coverage of aquatic species-specific assays is relatively scarce. Transient reporter gene assays could be a quick, economical, and reliable bridging technology. However, the user should be aware of potential pitfalls that are influenced by reporter vector geometry. Here, we report the development of an AhR-responsive transient reporter-gene assay in the permanent zebrafish hepatocytes cell line (ZFL). Additionally, we disclose how viral, constitutive promoters within reporter-gene assay cassettes induce squelching of the primary signal. To counter this, we designed a novel normalization vector, bearing an endogenous zebrafish-derived genomic promoter (zfEF1aPro), which rescues the squelching-delimited system, thus, giving new insights into the modulation of transient reporter systems under xenobiotic stress. Finally, we uncovered how the ubiquitously used ligand BNF promiscuously activates multiple toxicity pathways of the xenobiotic metabolism and cellular stress response in an orchestral manner, presumably leading to a concentration-related inhibition of the AhR/ARNT/XRE-toxicity pathway and non-monotonous concentration–response curves. We named such a multi-level inhibitory mechanism that might mask effects as “maisonette squelching.” Graphical abstract A transient reporter gene assay in zebrafish cell lines utilizing endogenous regulatory gene elements shows increased in vitro toxicity testing performance. Synthetic and constitutive promotors interfere with signal transduction (“squelching”) and might increase cellular stress (cytotoxicity). The squelching phenomenon might occur on multiple levels (toxicity pathway crosstalk and normalization vector), leading to a complete silencing of the reporter signal.
      PubDate: 2021-10-15
       
  • Serotonin type-3 receptor antagonists selectively kill melanoma cells
           through classical apoptosis, microtubule depolymerisation, ERK activation,
           and NF-κB downregulation

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      Abstract: Malignant melanoma is a highly metastatic tumour, resistant to treatment. Serotonin type-3 (5-HT3) receptor antagonists, such as tropisetron and ondansetron, are well-tolerated antiemetic drugs commonly used to prevent nausea caused by chemotherapy or radiotherapy. We investigated the anticancer effects of these drugs on melanoma cancer cell lines WM-266–4 and B16F10 with or without paclitaxel. We constructed IC50 curves and performed Chou–Talalay analysis, using data obtained with the MTT assay. Flow cytometry and fluorescent microscopy were used to examine characteristics of the cell cycle, cell death and cytoskeleton changes. Protein levels and activation were analysed by western blotting and molecular docking studies carried out. Data were analysed by one way ANOVA and post hoc testing. Ondansetron and tropisetron showed selective concentration-dependent cytotoxicity in melanoma cell lines WM-266–4 and B16F10. The effect in combination with paclitaxel was synergistic. The drugs did not cause cell cycle arrest but did promote characteristics of classical apoptosis, including accumulation of subG1 DNA, cleaved caspase-3, mitochondrial membrane permeability and phosphatidylserine exposure. As well, the cytosolic calcium level in the melanoma cells was enhanced, phosphorylated ERK1/2 induced and NF-κB inhibited. Finally, the formation of microtubules was shown to be impaired in melanoma cells treated with ondansetron or tropisetron. Docking studies were used to predict that these drugs could bind to the colchicine binding site on the tubulin molecule. Antiemetic drugs, already given in combination with chemotherapy, may enhance the cytotoxic effect of chemotherapy, following successful delivery to the tumour site.
      PubDate: 2021-10-15
       
  • METTL14 promotes doxorubicin-induced cardiomyocyte ferroptosis by
           regulating the KCNQ1OT1-miR-7-5p-TFRC axis

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      Abstract: Doxorubicin (DOX) has toxic effects on the heart, causing cardiomyopathy and heart injury, but the underlying mechanisms of these effects require further investigation. This study investigated the role of DOX in promoting ferroptosis to induce myocardial injury. AC16 cardiomyocyte and neonatal rat ventricle cardiomyocytes were used as an in vitro model to study the molecules involved in myocardial injury using gene silencing, ectopic expression, and RNA immunoprecipitation. Messenger RNA and protein level analyses showed that DOX treatment resulted in the upregulation of methyltransferase-like 14 (METTL14), which catalyzes the m6A modification of the long non-coding RNA KCNQ1OT1, a miR-7-5p sponge. The RNA-binding protein IGF2BP1 is associated with KCNQ1OT1 to increase its stability and robustly inhibit miR-7-5p activity. Furthermore, a lack of miR-7-5p expression led to increased levels of transferrin receptor, promoting the uptake of iron and production of lipid reactive oxygen species and demonstrating that DOX-induced ferroptosis occurs in AC16 cells. Additionally, we found that miR-7-5p targets METTL14 in AC16 cells. Meanwhile, the role of METTL14/KCNQ1OT1/miR-7-5p axis in regulating ferroptosis in neonatal rat ventricle cardiomyocytes was also confirmed. Our results indicate that selectively inhibiting ferroptosis mediated by a METTL14/KCNQ1OT1/miR-7-5p positive feedback loop in cardiomyocytes could provide a new therapeutic approach to control DOX-induced cardiac injury. Graphical abstract
      PubDate: 2021-10-14
       
  • Vitamin D3/VDR inhibits inflammation through NF-κB pathway accompanied by
           resisting apoptosis and inducing autophagy in abalone Haliotis discus
           hannai

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      Abstract: Vitamin D3 is believed to be a contributing factor to innate immunity. Vitamin D receptor (VDR) has a positive effect on inhibiting nuclear factor κB (NF-κB)-mediated inflammation. The underlying molecular mechanisms remain unclear, particularly in mollusks. Consequently, this study will investigate the process of vitamin D3/VDR regulating NF-κB pathway and further explore their functions on inflammation, autophagy, and apoptosis in abalone Haliotis discus hannai. Results showed that knockdown of VDR by using siRNA and dsRNA of VDR in vitro and in vivo led to more intense response of NF-κB signaling to lipopolysaccharide and higher level of apoptosis and autophagy. In addition, 1,25(OH)2D3 stimulation after VDR silencing could partially alleviate apoptosis and induce autophagy. Overexpression of VDR restricted the K48-polyubiquitin chain-dependent inhibitor of κB (IκB) ubiquitination and apoptosis-associated speck-like protein containing CARD (ASC) oligomerization. Besides, VDR silencing resulted in increase of ASC speck formation. In further mechanistic studies, we showed that VDR can directly bind to IκB and IKK1 in vitro and in vivo. In the feeding trial, H&E staining, TUNEL, and electron microscope results showed that vitamin D3 deficiency (0 IU/kg) could recruit more basophilic cells and increase more TUNEL-positive apoptotic cells and lipid droplets (LDs) than vitamin D3 supplement (1000 IU/kg and 5000 IU/kg). In summary, abalone VDR plays a negative regulator role in NF-κB-mediated inflammation via interacting with IκB and inhibiting ubiquitin-dependent degradation of IκB. Vitamin D3 in combination with VDR is essential to establish a delicate balance between autophagy and apoptosis in response to inflammation.
      PubDate: 2021-10-12
       
  • MMP-9 reinforces radiation-induced delayed invasion and metastasis of
           neuroblastoma cells through second-signaling positive feedback with NFκB
           via both ERK and IKK activation

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      Abstract: Neuroblastoma (NB) progression is branded with hematogenous metastasis and frequent relapses. Despite intensive multimodal clinical therapy, outcomes for patients with progressive disease remain poor, with negligible long-term survival. Therefore, understanding the acquired molecular rearrangements in NB cells with therapy pressure and developing improved therapeutic strategies is a critical need to improve the outcomes for high-risk NB patients. We investigated the rearrangement of MMP9 in NB with therapy pressure, and unveiled the signaling that facilitates NB evolution. Radiation-treatment (RT) significantly increased MMP9 expression/activity, and the induced enzyme activity was persistently maintained across NB cell lines. Furthermore, RT-triggered NFκB transcriptional activity and this RT-induced NFκB were required/adequate for MMP9 maintenance. RT-triggered NFκB-dependent MMP9 actuated a second-signaling feedback to NFκB, facilitating a NFκB-MMP9-NFκB positive feedback cycle (PFC). Critically, MMP9-NFκB feedback is mediated by MMP9-dependent activation of IKKβ and ERK phosphotransferase activity. Beyond its tumor invasion/metastasis function, PFC-dependent MMP9 lessens RT-induced apoptosis and favors survival pathway through the activation of NFκB signaling. In addition, PFC-dependent MMP9 regulates 19 critical molecular determinants that play a pivotal role in tumor evolution. Interestingly, seven of 19 genes possess NFκB-binding sites, demonstrating that MMP9 regulates these molecules by activating NFκB. Collectively, these data suggest that RT-triggered NFκB-dependent MMP9 actuates feedback to NFκB though IKKβ- and ERK1/2-dependent IκBα phosphorylation. This RT-triggered PFC prompts MMP9-dependent survival advantage, tumor growth, and dissemination. Targeting therapy-pressure-driven PFC and/or selective inhibition of MMP9 maintenance could serve as promising therapeutic strategies for treatment of progressive NB.
      PubDate: 2021-10-09
       
  • Suspension state and shear stress enhance breast tumor cells EMT through
           YAP by microRNA-29b

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      Abstract: Except for biochemical effects, suspension state (Sus) is proved to induce epithelial-mesenchymal transition (EMT) of circulating tumor cells (CTCs) mechanically. However, the difference between the effects of the mechanical microenvironment in capillaries (simplified as shear stress (SS) and Sus) and single Sus on EMT is unclear, nor the underlying mechanism. Here, breast tumor cells (BTCs) were loaded with Sus and SS to mimic the situation of CTCs stimulated by these two kinds of mechanics. It was demonstrated that the EMT of BTCs was enhanced by Sus and SS and the mechanotransductor yes-associated protein (YAP) was partially cytoplasmic stored with microRNA (miR)-29b decreased, which was detected by miR sequencing. Though it couldn’t possess a feedback regulation, YAP promoted miR-29b expression and posttranscriptionally regulated BTCs EMT through miR-29b, where transforming growth factor β involved. Analysis of clinical database showed that high miR-29b expression was beneficial to high survival rate stabilizing its role of tumor suppressor. This study discovers the mechanism that Sus and SS promote BTCs EMT by YAP through miR-29b posttranscriptionally and highlight the potential of YAP and miR-29b in tumor therapy. Graphical abstract The combination of suspension state and shear stress promotes transforming growth factor β involved epithelial-mesenchymal transition by yes-associated protein through microRNA-29b
      PubDate: 2021-10-07
       
  • Molecular implications of HOX genes targeting multiple signaling pathways
           in cancer

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      Abstract: Homeobox (HOX) genes encode highly conserved homeotic transcription factors that play a crucial role in organogenesis and tissue homeostasis. Their deregulation impacts the function of several regulatory molecules contributing to tumor initiation and progression. A functional bridge exists between altered gene expression of individual HOX genes and tumorigenesis. This review focuses on how deregulation in the HOX-associated signaling pathways contributes to the metastatic progression in cancer. We discuss their functional significance, clinical implications and ascertain their role as a diagnostic and prognostic biomarker in the various cancer types. Besides, the mechanism of understanding the theoretical underpinning that affects HOX-mediated therapy resistance in cancers has been outlined. The knowledge gained shall pave the way for newer insights into the treatment of cancer. Graphical abstract
      PubDate: 2021-10-06
       
  • E-cig vapor condensate alters proteome and lipid profiles of membrane
           rafts: impact on inflammatory responses in A549 cells

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      Abstract: Electronic cigarettes (e-cigs) are battery-operated heating devices that aerosolize e-liquid, typically containing nicotine and several other chemicals, which is then inhaled by a user. Over the past decade, e-cigs have gained immense popularity among both smokers and non-smokers. One reason for this is that they are advertised as a safe alternative to conventional cigarettes. However, the recent reports of e-cig use associated lung injury have ignited a considerable debate about the relative harm and benefits of e-cigs. The number of reports about e-cig-induced inflammation and pulmonary health is increasing as researchers seek to better understand the effects of vaping on human health. In line with this, we investigated the molecular events responsible for the e-cig vapor condensate (ECVC)–mediated inflammation in human lung adenocarcinoma type II epithelial cells (A549). In an attempt to limit the variables caused by longer ingredient lists of flavored e-cigs, tobacco-flavored ECVC (TF-ECVC±nicotine) was employed for this study. Interestingly, we observed significant upregulation of cytokines and chemokines (IL-6, IL-8, and MCP-1) in A549 cells following a 48 h TF-ECVC challenge. Furthermore, there was a significant increase in the expression of pattern recognition receptors TLR-4 and NOD-1, lipid raft–associated protein caveolin-1, and transcription factor NF-кB in TF-ECVC with and/or without nicotine-challenged lung epithelial cells. Our results further demonstrate the harboring of TLR-4 and NOD-1 in the caveolae of TF-ECVC-challenged A549 cells. Proteomic and lipidomic analyses of lipid raft fractions from control and challenged cells revealed a distinct protein and lipid profile in TF-ECVC (w/wo nicotine)-exposed A549 cells. Interestingly, the inflammatory effects of TF-ECVC (w/wo nicotine) were inhibited following the caveolin-1 knockdown, thus demonstrating a critical role of caveolae raft–mediated signaling in eliciting inflammatory responses upon TF-ECVC challenge. Graphical Graphical
      PubDate: 2021-10-01
       
  • The HNF1A-AS1/miR-92a-3p axis affects the radiosensitivity of non-small
           cell lung cancer by competitively regulating the JNK pathway

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      Abstract: Background It has been widely reported that long non-coding RNAs (lncRNAs) could affect the varieties of tumor response to radiotherapy. LncRNA HNF1A-AS1 is transcribed from HNF1A gene cluster’s antisense strand. This work focused on the mechanism of how HNF1A-AS1 participated in the radiosensitivity of non-small cell lung cancer (NSCLC). Methods The mRNA or protein expression of HNF1A-AS1, miR-92a-3p MAP2K4, and JNK in NSCLC cells and tissues was detected by qRT-PCR or western blotting. RNA immunoprecipitation (RIP) detection and luciferase reporting system were used to evaluate the relationship between HNFA-AS1 and miR-92a-3p or between miR-92a-3p and MAP2K4. Flow cytometry assays, colony formation, and MTT were performed to analyze the function changes in A549 and Calu-1 cells. The rescue experiment was also conducted to explore the underlying mechanisms. Results HNF1A-AS1 was investigated in NSCLC cells and tissues and highly related to the advanced pathological stage. HNF1A-AS1 bound with miR-92a-3p, which was downregulated in NSCLC. It showed that miR-92a-3p was negatively related to HNF1A-AS1. Knockdown of HNF1A-AS1 impacted most cell biological behaviors in NSCLC cells, including restricting the proliferation and aggravating apoptosis. Furthermore, knockdown of HNF1A-AS1 dramatically enhanced radiotherapy sensitivity of NSCLC. Moreover, miR-92a-3p was found to target MAP2K4 and could reduce MAP2K4 expression. Inhibition of HNF1A-AS1 elevated radiotherapy sensitivity and retarded the progression of NSCLC cells, followed by decreasing expression levels of MAP2K4. Besides, MAP2K4 mimic rescued the si-HNF1A-AS1 effects on the biological behavior of NSCLC cells. Conclusion HNF1A-AS1 is highly expressed in NSCLC. MiR-92a-3p is the target gene of HNF1A-AS1 and involved in tumor progression by regulating the MAP2K4/JNK pathway. HNF1AS1/miR-92a-3p/MAP2K4 axis plays important roles in radiotherapy resistance of NSCLC. Graphical abstract
      PubDate: 2021-10-01
       
  • Folic acid alleviates jaundice of phenylhydrazine (PHA)-induced neonatal
           rats by reducing Lys-homocysteinylation of albumin

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      Abstract: Neonatal jaundice is a common symptom that occurs in neonates during the first month of their life and is generally divided into physiological and pathological subtypes. In serious cases, pathological neonatal jaundice frequently shows complications including seizures, cerebral palsy, and kernicterus. However, due to the unclear pathogenesis of pathological neonatal jaundice, effective drugs for this disease remain unsatisfied. In the present study, we first estimated the protective effects of folic acid (FA) on phenylhydrazine (PHA) or homocysteine (Hcy)-injected neonatal rats (2–3 days aged). Intriguingly, we found that FA significantly decreased the elevated total bilirubin (TBIL) and direct bilirubin (DBIL) concentration, alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) activity in PHA- or Hcy-injected rats, indicating that FA improves liver functions. Meanwhile, our results also showed that the plasma Hcy level and N-homocysteinylation (N-Hcy) modification of albumin were significantly elevated in the jaundice rats, which were obviously reversed after FA administration. Furthermore, we identified a novel N-Hcy modification site K545 of human serum albumin (HSA) using LC-MS/MS, and the mutagenesis assay in HEK293 further validated these observations. Besides, we demonstrated that the N-Hcy modification of albumin functionally inhibits the bilirubin-binding ability of albumin without altering its protein level both in vitro and in vivo. Altogether, we highlight a mechanism that FA reduces the plasma Hcy level and thereby enhance the bilirubin-binding ability of albumin, which may provide a novel therapeutic strategy for the treatment of pathological neonatal jaundice. Graphical abstract
      PubDate: 2021-10-01
       
  • Pyruvate kinase M2 in chronic inflammations: a potpourri of crucial
           protein–protein interactions

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      Abstract: Chronic inflammation (CI) is a primary contributing factor involved in multiple diseases like cancer, stroke, diabetes, Alzheimer’s disease, allergy, asthma, autoimmune diseases, coeliac disease, glomerulonephritis, sepsis, hepatitis, inflammatory bowel disease, reperfusion injury, and transplant rejections. Despite several expansions in our understanding of inflammatory disorders and their mediators, it seems clear that numerous proteins participate in the onset of CI. One crucial protein pyruvate kinase M2 (PKM2) much studied in cancer is also found to be inextricably woven in the onset of several CI’s. It has been found that PKM2 plays a significant role in several disorders using a network of proteins that interact in multiple ways. For instance, PKM2 forms a close association with epidermal growth factor receptors (EGFRs) for uncontrolled growth and proliferation of tumor cells. In neurodegeneration, PKM2 interacts with apurinic/apyrimidinic endodeoxyribonuclease 1 (APE1) to onset Alzheimer’s disease pathogenesis. The cross-talk of protein tyrosine phosphatase 1B (PTP1B) and PKM2 acts as stepping stones for the commencement of diabetes. Perhaps PKM2 stores the potential to unlock the pathophysiology of several diseases. Here we provide an overview of the notoriously convoluted biology of CI’s and PKM2. The cross-talk of PKM2 with several proteins involved in stroke, Alzheimer’s, cancer, and other diseases has also been discussed. We believe that considering the importance of PKM2 in inflammation-related diseases, new options for treating various disorders with the development of more selective agents targeting PKM2 may appear. Graphical abstract
      PubDate: 2021-10-01
       
  • Inhibition of ER stress attenuates kidney injury and apoptosis induced by
           3-MCPD via regulating mitochondrial fission/fusion and Ca2+ homeostasis

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      Abstract: 3-Chloro-1, 2-propanediol (3-MCPD) is a food-borne toxic substance well-known for more than 40 years that is mainly associated with nephrotoxicity. A better understanding of 3-MCPD nephrotoxicity is required to devise efficacious strategies to counteract its toxicity. In the present work, the role of endoplasmic reticulum (ER) stress along with its underlying regulatory mechanism in 3-MCPD-mediated renal cytotoxicity was investigated in vivo and in vitro. Our data indicated that 3-MCPD-stimulated ER stress response evidenced by sustained activation of PERK-ATF4-p-CHOP and IRE1 branches in Sprague Dawley (SD) rats and human embryonic kidney (HEK293) cells. Moreover, ER stress-associated specific apoptotic initiator, caspase 12, was over-expressed. Blocking ER stress with its antagonist, 4-phenylbutyric acid (4-PBA), improved the morphology and function of kidney effectively. 4-PBA also increased cell viability, relieved mitochondrial vacuolation, and inhibited cell apoptosis through regulating caspase-dependent intrinsic apoptosis pathways. Furthermore, the enhanced expressions of two mitochondrial fission proteins, DRP1/p-DRP1 and FIS1, and the relocation of DRP1 on mitochondria subjected to 3-MPCD were reversed by 4-PBA, while the expression of the fusion protein, MFN2, was restored. Moreover, cellular Ca2+ overload, the over-expression of CaMKK2, and the loss of mitochondria-associated membranes (MAM) were also relieved after 4-PBA co-treatment. Collectively, our data emphasized that ER stress plays critical role in 3-MCPD-mediated mitochondrial dysfunction and subsequent apoptosis as well as blockage of ER stress ameliorated kidney injury through improving mitochondrial fission/fusion and Ca2+ homeostasis. These findings provide a novel insight into the regulatory role of ER stress in 3-MCPD-associated nephropathy and a potential therapeutic strategy. Graphical abstract Graphical Headlights 1. 4-PBA inhibits ER stress mainly through regulating PERK-ATF4-CHOP and IRE1-XBP1s branches. 2. Inhibition of ER stress by 4-PBA mitigates ER associated and mitochondrial apoptosis 3. Inhibition of ER stress by 4-PBA helps maintaining calcium homeostasis and mitochondrial dynamic.
      PubDate: 2021-10-01
       
  • The DNA methylation inhibitor RG108 protects against noise-induced hearing
           loss

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      Abstract: Background Noise-induced hearing loss represents a commonly diagnosed type of hearing disability, severely impacting the quality of life of individuals. The current work is aimed at assessing the effects of DNA methylation on noise-induced hearing loss. Methods Blocking DNA methyltransferase 1 (DNMT1) activity with a selective inhibitor RG108 or silencing DNMT1 with siRNA was used in this study. Auditory brainstem responses were measured at baseline and 2 days after trauma in mice to assess auditory functions. Whole-mount immunofluorescent staining and confocal microcopy of mouse inner ear specimens were performed to analyze noise-induced damage in cochleae and the auditory nerve at 2 days after noise exposure. Results The results showed that noise exposure caused threshold elevation of auditory brainstem responses and cochlear hair cell loss. Whole-mount cochlea staining revealed a reduction in the density of auditory ribbon synapses between inner hair cells and spiral ganglion neurons. Inhibition of DNA methyltransferase activity via a non-nucleoside specific pharmacological inhibitor, RG108, or silencing of DNA methyltransferase-1 with siRNA significantly attenuated ABR threshold elevation, hair cell damage, and the loss of auditory synapses. Conclusions This study suggests that inhibition of DNMT1 ameliorates noise-induced hearing loss and indicates that DNMT1 may be a promising therapeutic target. Graphical abstract Graphical Headlights • RG108 protected against noise-induced hearing loss • RG108 administration protected against noise-induced hair cell loss and auditory neural damage. • RG108 administration attenuated oxidative stress-induced DNA damage and subsequent apoptosis-mediated cell loss in the cochlea after noise exposure.
      PubDate: 2021-10-01
       
  • ZNF471 modulates EMT and functions as methylation regulated tumor
           

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      Abstract: Cervical cancer (CC) is a leading cause of cancer-related death among women in developing countries. However, the underlying mechanisms and molecular targets for therapy remain to be fully understood. We investigated the epigenetic regulation, biological functions, and clinical utility of zinc-finger protein 471 (ZNF471) in CC. Analysis of cervical tissues and five independent public datasets of CC showed significant hypermethylation of the ZNF471 gene promoter. In CC cell lines, promoter DNA methylation was inversely correlated with ZNF471 expression. The sensitivity and specificity of the ZNF471 hypermethylation for squamous intraepithelial lesion (SIL) vs tumor and normal vs tumor was above 85% with AUC of 0.937. High methylation and low ZNF471 expression predicted poor overall and recurrence-free survival. We identified −686 to +114 bp as ZNF471 promoter, regulated by methylation using transient transfection and luciferase assays. The promoter CpG site methylation of ZNF471 was significantly different among cancer types and tumor grades. Gal4-based heterologous luciferase reporter gene assays revealed that ZNF471 acts as a transcriptional repressor. The retroviral mediated overexpression of ZNF471 in SiHa and CaSki cells inhibited growth, proliferation, cell migration, invasion; delayed cell cycle progression in vitro by increasing cell doubling time; and reduced tumor growth in vivo in nude mice. ZNF471 overexpression inhibited key members of epithelial-mesenchymal transition (EMT), Wnt, and PI3K-AKT signaling pathways. ZNF471 inhibited EMT by directly targeting vimentin as analyzed by bioinformatic analysis, ChIP-PCR, and western blotting. Thus, ZNF471 CpG specific promoter methylation may determine the prognosis of CC and could function as a potential tumor suppressor by targeting EMT signaling.
      PubDate: 2021-10-01
       
  • High-content screening of diterpenoids from Isodon species as autophagy
           modulators and the functional study of their antiviral activities

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      Abstract: Autophagy is a conserved lysosomal degradation process, and abnormal autophagy has been associated with various pathological processes, e.g., neurodegeneration, cancer, and pathogen infection. Small chemical modulators of autophagy show the potential to treat autophagy-associated diseases. Diterpenoids, nature products found in various plants, exhibit a wide range of bioactivity, and we have recently isolated and characterized over 150 diterpenoids from Isodon species distributed in China. Here, we applied a high-content fluorescence imaging-based assay to assess these diterpenoids’ ability to affect autophagic flux in HeLa cells. We found that enanderinanin J, an ent-kauranoid dimer, is an autophagy inhibitor, manifested by its ability to increase lysosomal pH and inhibit the fusion between autophagosomes and lysosomes. Autophagy has been shown to be either positively or negatively involved in the life cycle of Zika virus (ZIKV), Japanese encephalitis virus (JEV), Dengue virus (DENV), and enterovirus-A71 (EV-A71). We found that enanderinanin J significantly inhibited the infection of ZIKV, DENV, JEV, or EV-A71. Interestingly, although ATG5 knockdown inhibited ZIKV or JEV infection, enanderinanin J further inhibited the infection of ZIKV or JEV in ATG5-knockdown cells. Taken together, our data indicate that enanderinanin J inhibits autophagosome-lysosome fusion and is a potential antiviral agent. Graphical abstract
      PubDate: 2021-10-01
       
  • MS4A3-HSP27 target pathway reveals potential for haematopoietic disorder
           treatment in alimentary toxic aleukia

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      Abstract: Alimentary toxic aleukia (ATA) is correlated with consuming grains contaminated by Fusarium species, particularly T-2 toxin, which causes serious hurt to human and animal health, chiefly in disorders of the haematopoietic system. However, the mechanism of haematopoietic dysfunction induced by T-2 toxin and the possible target pathway for the treatment of T-2 toxin-induced haematopoietic disorder of ATA remains unclear. In this study, genomes and proteomics were used for the first time to investigate the key differential genes and proteins that inhibit erythroid differentiation of K562 cells caused by T-2 toxin, and it was found that heat shock protein 27 (HSP27) and membrane-spanning 4-domains, subfamily A, member 3 (MS4A3) may play an important role in erythroid differentiation. Meanwhile, MS4A3 interference can inhibit the occurrence of erythroid differentiation of K562 cells and promote the phosphorylation of HSP27. Moreover, the binding of HSP27 to MS4A3 in natural state can activate the phosphorylation site of HSP27 (Ser-83), while T-2 toxin can abolish the activation of phosphorylation site by inhibiting the expression of MS4A3. These findings for the first time demonstrated that the MS4A3-HSP27 pathway may function an efficient therapeutic target pathway for treating T-2 toxin elicited haematopoietic disorders of ATA. Graphical abstract
      PubDate: 2021-09-28
       
  • Cadmium affects autophagy in the human intestinal cells Caco-2 through
           ROS-mediated ERK activation

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      Abstract: Cadmium is a toxic metal that enters the food chain. Following oral ingestion, the intestinal epithelium has the capacity to accumulate high levels of this metal. We have previously shown that Cd induces ERK1/2 activation in differentiated but not proliferative human enterocytic-like Caco-2 cells. As autophagy is a dynamic process that plays a critical role in intestinal mucosa, we aimed the present study 1) to investigate the role of p-ERK1/2 in constitutive autophagy in proliferative Caco-2 cells and 2) to investigate whether Cd-induced activation of ERK1/2 modifies autophagic activity in postconfluent Caco-2 cell monolayers. Western blot analyses of ERK1/2 and autophagic markers (LC3, SQSTM1), and cellular staining with acridine orange showed that ERK1/2 and autophagic activities both decreased with time in culture. GFP-LC3 fluorescence was also associated with proliferative cells and the presence of a constitutive ERK1/2-dependent autophagic flux was demonstrated in proliferative but not in postconfluent cells. In the latter condition, serum and glucose deprivation triggered autophagy via a transient phosphorylation of ERK1/2, whereas Cd-modified autophagy via a ROS-dependent sustained activation of ERK1/2. Basal autophagy flux in proliferative cells and Cd-induced increases in autophagic markers in postconfluent cells both involved p-ERK1/2. Whether Cd blocks autophagic flux in older cell cultures remains to be clarified but our data suggest dual effects. Our results prompt further studies investigating the consequences that Cd-induced ERK1/2 activation and the related effect on autophagy may have on the intestinal cells, which may accumulate and trap high levels of Cd under some nutritional conditions. Graphical abstract
      PubDate: 2021-09-28
       
  • Phototoxicity-free blue light for enhancing therapeutic angiogenic
           efficacy of stem cells

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      Abstract: Low-level light therapy (LLLT) is a safe and noninvasive technique that has drawn attention as a new therapeutic method to treat various diseases. However, little is known so far about the effect of blue light for LLLT due to the generation of reactive oxygen species (ROS) that can cause cell damage. We introduced a blue organic light-emitting diode (bOLED) as a safe and effective light source that could generate a low amount of heat and luminance compared to conventional light sources (e.g., light-emitting diodes). We compared phototoxicity of bOLED light with different light fluences to human adipose-derived stem cells (hADSC). We further explored molecular mechanisms involved in the therapeutic efficacy of bOLED for enhancing angiogenic properties of hADSC, including intracellular ROS control in hADSCs. Using optimum conditions of bOLED light proposed in this study, photobiomodulation and angiogenic properties of hADSCs were enhanced. These findings might open new methods for using blue light in LLLT. Such methods can be implemented in future treatments for ischemic disease. Graphical abstract
      PubDate: 2021-09-28
       
  • LINC01089, suppressed by YY1, inhibits lung cancer progression by
           targeting miR-301b-3p/HPDG axis

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      Abstract: Purpose LINC01089 is a newly identified lncRNA and rarely reported in human cancers. Our study aimed to investigate its role in lung cancer. Methods YY1, LINC01089, and miR-301b-3p levels in lung cancer tissues and cells were assessed using qRT-PCR. Bioinformatics analysis and luciferase reporter, ChIP, and RIP assays were carried out for determining the relationships among YY1, LINC01089, miR-301b-3p, and HPGD. Gain- and loss-of-function assays were carried out to confirm the impacts of LINC01089 and HPDG in lung cancer cells. CCK-8 assay was used to assess cell proliferation rate, and Transwell assay was applied to measure cell invasion and migration. An in vivo tumor model was applied for validating the role of LINC01089. Results LINC01089 was decreased in lung cancer tissues and cells, and low LINC01089 level predicted a poor clinical outcome. YY1 directly bound to LINC01089 promoter region and inhibited its transcription. LINC01089 knockdown thwarted the proliferation, invasion, and migration capacity of H1299 and A549 cells and aggravated tumor growth. Specifically, LINC01089 functioned as a competing endogenous RNA of miR-301b-3p to modulate HPGD and thereby affected lung cancer progression. Conclusion Our data revealed that LINC01089, directly suppressed by YY1, inhibited lung cancer progression by targeting the miR-301b-3p/HPGD axis. Graphical abstract 1. LINC01089 expression was downregulated in lung cancer tisuues and cell lines, and low LINC01089 levels predicted a poor clinical outcome. 2. LINC01089 knockdown enhanced proliferation, invasion, and migration of H1299 and A549 cells in vitro and promoted lung cancer cell tumorigenesis and metastasis in vivo. 3. LINC01089, directly suppressed by YY1, functioned as a competing endogenous RNA against miR-301b-3p to increase HPGD expression.
      PubDate: 2021-09-24
       
 
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