JournalTOCs

Biochemistry and Cell Biology
Journal Prestige (SJR): 0.856

Citation Impact (citeScore): 2
Number of Followers: 18

Hybrid journal (It can contain Open Access articles)
ISSN (Print) 0829-8211 - ISSN (Online) 1208-6002
Published by NRC Research Press

[19 journals]

Dysregulation of insulin-like growth factor-1 signaling in postnatal bone
elongation
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  Authors: Cassaundra A. White, Maria A. Serrat
  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  Insulin-like growth factor-1 (IGF-1) is a critical modulator of cell growth and survival, making it a central part of maintaining essentially every biological system in the body. Knowledge of the intricate mechanisms involved in activating IGF-1 signaling is not only key to understanding basic processes of growth and development, but also for addressing diseases, such as cancer and diabetes. This brief review explores how dysregulation of normal IGF-1 signaling can impact growth by examining its role in postnatal bone elongation. IGF-1 actions are dysregulated in autoimmune diseases, such as juvenile idiopathic arthritis and chronic kidney disease, which results in growth stunting. Conversely, childhood obesity results in growth acceleration, premature growth cessation, and ultimately, diminished bone quality, while systemic IGF-1 levels remain normal. Understanding the role of IGF-1 signaling in normal and dysregulated growth can add to other studies that address how this system regulates chronic diseases.
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-05-29T07:00:00Z
  DOI: 10.1139/bcb-2023-0025
Remembering the legacy of Professor Mohammad Hashemi: a pioneer in
molecular genetic studies in southeast Iran (1965–2019)
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  Authors: Farhad Tabasi, Ebrahim Eskandari, Saeid Ghavmi
  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  Professor Mohammad Hashemi was a clinical biochemist and cancer genetic scientist. He has been chair and head of Department of Clinical Biochemistry at Zahedan University of Medical Sciences, Zahedan, Iran. He has played an important role in the improvement of understanding of genetics of disease in southeast Iran. He was also a part of international team for the discovery of the role of calprotectin (S100A8/A9) in cancer biology via regulation of cell fate in tumor cells. He had over 300 peer-reviewed scientific publications and trained significant numbers of high quality personals (>40) in the field of biomedical sciences. His sudden death in 2019 shocked national and international scientific society but his scientific legacy will remain alive forever.
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-05-29T07:00:00Z
  DOI: 10.1139/bcb-2023-0116
Message from Dr. Philippe T. Georgel, Guest Editor for the Marshall
University Collection, Brad D. Smith, President of Marshall University,
and Dr. Anivandan Mukherjee, Provost of Marshall University
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  Authors: Philippe T. Georgel, Brad D. Smith, Avinandan Mukherjee
  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-04-13T07:00:00Z
  DOI: 10.1139/bcb-2023-0072
Evaluation of biochemical profile and oxidative damage to lipids and
proteins in patients with lysosomal acid lipase deficiency
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  Authors: Gilian Guerreiro, Marion Deon, Carmen Regla Vargas
  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  Lysosomal acid lipase deficiency (LALD) is an inborn error of metabolism that lacks satisfactory treatment, which leads to the development of severe hepatic and cardiac complications and may even lead to death. In this sense, knowledge of the mechanisms involved in the pathophysiology of this disorder becomes essential to allow the search for new therapeutic strategies. There are no studies in the literature investigating the role of reactive species and inflammatory processes in the pathophysiology of this disorder. Therefore, the aim of this work was to investigate parameters of oxidative and inflammatory stress in LALD patients. In this work, we obtained results that demonstrate that LALD patients are susceptible to oxidative stress caused by an increase in the production of free radicals, observed by the increase of 2-7-dihydrodichlorofluorescein. The decrease in sulfhydryl content reflects oxidative damage to proteins, as well as a decrease in antioxidant defenses. Likewise, the increase in urinary levels of di-tyrosine observed also demonstrates oxidative damage to proteins. Furthermore, the determination of chitotriosidase activity in the plasma of patients with LALD was significantly higher, suggesting a pro-inflammatory state. An increase in plasma oxysterol levels was observed in patients with LALD, indicating an important relationship between this disease and cholesterol metabolism and oxidative stress. Also, we observed in LALD patients increased levels of nitrate production. The positive correlation found between oxysterol levels and activity of chitotriosidase in these patients indicates a possible link between the production of reactive species and inflammation. In addition, an increase in lipid profile biomarkers such as total and low-density lipoprotein cholesterol were demonstrated in the patients, which reinforces the involvement of cholesterol metabolism. Thus, we can assume that, in LALD, oxidative and nitrosative damage, in addition to inflammatory process, play an important role in its evolution and future clinical manifestations. In this way, we can suggest that the study of the potential benefit of the use of antioxidant and anti-inflammatory substances as an adjuvant tool in the treatment will be important, which should be associated with the already recommended therapy.
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-04-12T07:00:00Z
  DOI: 10.1139/bcb-2022-0330
Expression of concern: MicroRNA-518-3p suppresses cell proliferation,
invasiveness, and migration in colorectal cancer via targeting TRIP4
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  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-04-12T07:00:00Z
  DOI: 10.1139/bcb-2023-0097
Analysis of financial challenges faced by graduate students in Canada
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  Authors: Sarah Jane Laframboise, Thomas Bailey, Anh-Thu Dang, Mercedes Rose, Zier Zhou, Matthew D. Berg, Stephen Holland, Sami Aftab Abdul, Kaela O'Connor, Sara El-Sahli, Dominique M. Boucher, Garrett Fairman, Jacky Deng, Katherine Shaw, Nathaniel Noblett, Alexa D’Addario, Madelaine Empey, Keaton Sinclair
  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  Graduate students are vital to the creation of research and innovation in Canada. The National Graduate Student Finance Survey was launched in 2021 by the Ottawa Science Policy Network to investigate the financial realities of Canadian graduate students. Closing in April 2022, the survey received 1305 responses from graduate students representing various geographical locations, years of study, fields of education, and demographic backgrounds. The results capture a snapshot into graduate student finances, including an in-depth analysis of stipends, scholarships, debt, tuition, and living expenses. In its entirety, we found that the majority of graduate students are facing serious financial concerns. This is largely due to stagnant funding for students both from federal and provincial granting agencies and from within their institutions. This reality is even worse for international students, members of historically underrepresented communities, and those with dependents, all of whom experience additional challenges that impact their financial security. Based on our findings, we propose several recommendations to the Tri-Council agencies (Natural Sciences and Engineering Research Council, Social Science and Humanities Research Council, and Canadian Institute for Health Research) and academic institutions to strengthen graduate student finances and help sustain the future of research in Canada.
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-04-11T07:00:00Z
  DOI: 10.1139/bcb-2023-0021
Retraction: Profibrogenic phenotype in caveolin-1 deficiency via
differential regulation of STAT-1/3 proteins
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  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-04-11T07:00:00Z
  DOI: 10.1139/bcb-2023-0089
Mechanism of myocardial fibrosis regulation by IGF-1R in atrial
fibrillation through the PI3K/Akt/FoxO3a pathway
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  Authors: Pei Zhang, Huilin Li, An Zhang, Xiao Wang, Qiyuan Song, Zhan Li, Weizong Wang, Jingwen Xu, Yinglong Hou, Yong Zhang
  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  Atrial structural remodeling takes on a critical significance to the occurrence and maintenance of atrial fibrillation (AF). As revealed by recent data, insulin-like growth factor-1 receptor (IGF-1R) plays a certain role in tissue fibrosis. In this study, the mechanism of IGF-1R in atrial structural remodeling was examined based on in vivo and in vitro experiments. First, cluster analysis of AF hub genes was conducted, and then the molecular mechanism was proposed by which IGF-1R regulates myocardial fibrosis via the PI3K/Akt/FoxO3a pathway. Subsequently, the mentioned mechanism was verified in human cardiac fibroblasts (HCFs) and rats transduced with IGF-1 overexpression type 9 adeno-associated viruses. The results indicated that IGF-1R activation up-regulated collagen Ⅰ protein expression and Akt phosphorylation in HCFs and rat atrium. The administration of LY294002 reversed the above phenomenon, improved the shortening of atrial effective refractory period, and reduced the increased incidence of AF and atrial fibrosis in rats. The transfection of FoxO3a siRNA reduced the anti-fibrotic effect of LY294002 in HCFs. The above data revealed that activation of IGF-1R takes on a vital significance to atrial structural remodeling by facilitating myocardial fibrosis and expediting the occurrence and maintenance of AF through the regulation of the PI3K/Akt/FoxO3a signaling pathway.
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-04-05T07:00:00Z
  DOI: 10.1139/bcb-2022-0199
AKT1 participates in ferroptosis vulnerability by driving autophagic
degradation of FTH1 in cisplatin-resistant ovarian cancer
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  Authors: Zhikun Shi, Hao Yuan, Lanqing Cao, Yang Lin
  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  Resistance to cisplatin (DDP)-based chemotherapy is an important reason for the failure of ovarian cancer treatment. However, tumor cells resistant to chemotherapy may expose vulnerability to other cell death pathways. Here, we found that DDP-resistant ovarian cancer cells are more susceptible to erastin-induced ferroptosis. It should be noted that this vulnerability does not depend on the weakening of classical ferroptosis defense proteins, but is caused by the reduction of ferritin heavy chain (FTH1). DDP-resistant ovarian cancer cells maintain a high level of autophagy to escape the pressure of chemotherapy, which ultimately leads to increased autophagic degradation of FTH1. We further revealed that the loss of AKT1 was the reason for the increased autophagy level of DDP-resistant ovarian cancer cells. Our study provides new insights into reversing DDP resistance in ovarian cancer by targeting ferroptosis pathway, and AKT1 may be a molecular marker of susceptibility to ferroptosis.
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-04-03T07:00:00Z
  DOI: 10.1139/bcb-2022-0361
Telomere biology and ribosome biogenesis: structural and functional
interconnections
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  Authors: Liia R. Valeeva, Liliia R. Abdulkina, Inna A. Agabekian, Eugene V. Shakirov
  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  Telomeres are nucleoprotein structures that play a pivotal role in the protection and maintenance of eukaryotic chromosomes. Telomeres and the enzyme telomerase, which replenishes telomeric DNA lost during replication, are important factors necessary to ensure continued cell proliferation. Cell proliferation is also dependent on proper and efficient protein synthesis, which is carried out by ribosomes. Mutations in genes involved in either ribosome biogenesis or telomere biology result in cellular abnormalities and can cause human genetic diseases, defined as ribosomopathies and telomeropathies, respectively. Interestingly, recent discoveries indicate that many of the ribosome assembly and rRNA maturation factors have additional noncanonical functions in telomere biology. Similarly, several key proteins and enzymes involved in telomere biology, including telomerase, have unexpected roles in rRNA transcription and maturation. These observations point to an intriguing cross-talk mechanism potentially explaining the multiple pleiotropic symptoms of mutations in many causal genes identified in various telomeropathy and ribosomopathy diseases. In this review, we provide a brief summary of eukaryotic telomere and rDNA loci structures, highlight several universal features of rRNA and telomerase biogenesis, evaluate intriguing interconnections between telomere biology and ribosome assembly, and conclude with an assessment of overlapping features of human diseases of telomeropathies and ribosomopathies.
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-03-29T07:00:00Z
  DOI: 10.1139/bcb-2022-0383
Astrocyte-specific Ca2+ activity: Mechanisms of action, experimental
tools, and roles in ethanol-induced dysfunction
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  Authors: O.R. Coulter, C.D. Walker, M.-L. Risher
  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  Astrocytes are a subtype of non-neuronal glial cells that reside in the central nervous system. Astrocytes have extensive peripheral astrocytic processes that ensheathe synapses to form the tripartite synapse. Through a multitude of pathways, astrocytes can influence synaptic development and structural maturation, respond to neuronal signals, and modulate synaptic transmission. Over the last decade, strong evidence has emerged demonstrating that astrocytes can influence behavioral outcomes in various animal models of cognition. However, the full extent of how astrocytes influence brain function is still being revealed. Astrocyte calcium (Ca2+) signaling has emerged as an important driver of astrocyte-neuronal communication allowing intricate crosstalk through mechanisms that are still not fully understood. Here, we will review the field's current understanding of astrocyte Ca2+ signaling and discuss the sophisticated state-of-the-art tools and approaches used to continue unraveling astrocytes' interesting role in brain function. Using the field of pre-clinical ethanol (EtOH) studies in the context of alcohol use disorder, we focus on how these novel approaches have helped to reveal an important role for astrocyte Ca2+ function in regulating EtOH consumption and how astrocyte Ca2+ dysfunction contributes to the cognitive deficits that emerge after EtOH exposure in a rodent model.
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-03-29T07:00:00Z
  DOI: 10.1139/bcb-2023-0008
Retraction: Wnt5A regulates the expression of ROR2 tyrosine kinase
receptor in ovarian cancer cells
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  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-03-28T07:00:00Z
  DOI: 10.1139/bcb-2023-0066
Retraction: MiR-204 suppresses cell proliferation and promotes apoptosis
in ovarian granulosa cells via targeting TPT1 in polycystic ovary syndrome
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  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-03-28T07:00:00Z
  DOI: 10.1139/bcb-2023-0070
Retraction: Role of the TSLP–DC–OX40L pathway in asthma pathogenesis
and airway inflammation in mice
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  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-03-28T07:00:00Z
  DOI: 10.1139/bcb-2023-0071
Retraction: MiR-301b promotes the proliferation, mobility, and
epithelial-to-mesenchymal transition of bladder cancer cells by targeting
EGR1
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  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-03-28T07:00:00Z
  DOI: 10.1139/bcb-2023-0074
Retraction: MicroRNA-181 inhibits proliferation and promotes apoptosis of
chondrocytes in osteoarthritis by targeting PTEN
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  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-03-27T07:00:00Z
  DOI: 10.1139/bcb-2023-0069
Retraction: Lentivirus-mediated angiopoietin-2 gene silencing decreases
TNF-α induced apoptosis of alveolar epithelium cells
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  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-03-24T07:00:00Z
  DOI: 10.1139/bcb-2023-0068
Retraction: Interaction between miR-572 and PPP2R2C, and their effects on
the proliferation, migration, and invasion of nasopharyngeal carcinoma
(NPC) cells
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  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-03-23T07:00:00Z
  DOI: 10.1139/bcb-2023-0061
High concentrations of fructose cause brain damage in mice
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  Authors: Anderson Cargnin-Carvalho, Mariella Reinol da Silva, Ana Beatriz Costa, Nicole Alessandra Engel, Bianca Xavier Farias, Joice Benedet Bressan, Kassiane Mathiola Backes, Francielly de Souza, Naiana da Rosa, Aloir Neri de Oliveira Junior, Mariana Pereira de Souza Goldim, Maria Eduarda Anastácio Borges Correa, Ligia Milanez Venturini, Jucélia Jeremias Fortunato, Josiane Somariva Prophiro, Fabrícia Petronilho, Paulo Cesar Lock Silveira, Gabriela Kozuchovsk Ferreira, Gislaine Tezza Rezin
  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  Excessive fructose consumption is associated with the incidence of obesity and systemic inflammation, resulting in increased oxidative damage and failure to the function of brain structures. Thus, we hypothesized that fructose consumption will significantly increase inflammation, oxidative damage, and mitochondrial dysfunction in the mouse brain and, consequently, memory damage. The effects of different fructose concentrations on inflammatory and biochemical parameters in the mouse brain were evaluated. Male Swiss mice were randomized into four groups: control, with exclusive water intake, 5%, 10%, and 20% fructose group. The 10% and 20% fructose groups showed an increase in epididymal fat, in addition to higher food consumption. Inflammatory markers were increased in epididymal fat and in some brain structures. In the evaluation of oxidative damage, it was possible to observe significant increases in the hypothalamus, prefrontal cortex, and hippocampus. In the epididymal fat and in the prefrontal cortex, there was a decrease in the activity of the mitochondrial respiratory chain complexes and an increase in the striatum. Furthermore, short memory was impaired in the 10% and 20% groups but not long memory. In conclusion, excess fructose consumption can cause fat accumulation, inflammation, oxidative damage, and mitochondrial dysfunction, which can damage brain structures and consequently memory.
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-03-22T07:00:00Z
  DOI: 10.1139/bcb-2022-0088
SARS-CoV-2 E protein-induced THP-1 pyroptosis is reversed by Ruscogenin
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  Authors: Houda Huang, Xiuzhen Li, Duoduo Zha, Hongru Lin, Lingyi Yang, Yihan Wang, Luyan Xu, Linsiqi Wang, Tianhua Lei, Zhou Zhou, Yun-Fei Xiao, Hong-Bo Xin, Mingui Fu, Yisong Qian
  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), an emerging pathogenic coronavirus, has been reported to cause excessive inflammation and dysfunction in multiple cells and organs, but the underlying mechanisms remain largely unknown. Here we showed exogenous addition of SARS-CoV-2 envelop protein (E protein) potently induced cell death in cultured cell lines, including THP-1 monocytic leukemia cells, endothelial cells, and bronchial epithelial cells, in a time- and concentration-dependent manner. SARS-CoV-2 E protein caused pyroptosis-like cell death in THP-1 and led to GSDMD cleavage. In addition, SARS-CoV-2 E protein upregulated the expression of multiple pro-inflammatory cytokines that may be attributed to activation of NF-κB, JNK and p38 signal pathways. Notably, we identified a natural compound, Ruscogenin, effectively reversed E protein-induced THP-1 death via inhibition of NLRP3 activation and GSDMD cleavage. In conclusion, these findings suggested that Ruscogenin may have beneficial effects on preventing SARS-CoV-2 E protein-induced cell death and might be a promising treatment for the complications of COVID-19.
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-03-16T07:00:00Z
  DOI: 10.1139/bcb-2022-0359
Hedgehog signal activates AMPK via Smoothened to promote autophagy and
lipid degradation in hepatocytes
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  Authors: Yixing Yao, Tianyuan Li, Tingting Yu, Xin Yang, Yue Wang, Jing Cai, Steven Y. Cheng, Chen Liu, Shen Yue
  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  Studies in the past decade have shown that lipid droplets stored in liver cells under starvation are encapsulated by autophagosomes and fused to lysosomes via the endocytic system. Autophagy responds to a variety of environmental factors inside and outside the cell, so it has a complex signal regulation network. To this end, we first explored the role of Hedgehog (Hh) in autophagy and lipid metabolism. Treatment of normal mouse liver cells with SAG and GDC-0449 revealed elevated phosphorylation of AMP-activated protein kinase (AMPK) and increased lipidation of LC3. SAG, and GDC-0449 were agonist and antagonist of Smoothened (Smo) in canonical Hh pathway, respectively, but they played a consistent role in the regulation of autophagy in hepatocytes. Moreover, SAG and GDC-0449 did not affect the expression of glioma-associated oncogene (Gli1) and patched 1, suggesting the absence of canonical Hh signaling in hepatocytes. We further knocked down the Smo and found that the effects of SAG and GDC-0449 disappeared, indicating that the non-canonical Smo pathway was involved in the regulation of autophagy in hepatocytes. In addition, SAG and GDC-0449 promoted lipid degradation and inhibited lipid production signals. Knockdown of Smo slowed down the rate of lipid degradation rather than Sufu or Gli1, indicating that Hh signaling regulated the lipid metabolism via Smo. In summary, activates AMPK via Smo to promote autophagy and lipid degradation.
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-02-23T08:00:00Z
  DOI: 10.1139/bcb-2022-0345
Mitogen- and stress-activated protein kinase (MSK1/2) regulated gene
expression in normal and disease states
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  Authors: Hedieh Sattarifard, Akram Safaei, Enzhe Khazeeva, Mojgan Rastegar, James R. Davie
  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  The mitogen- and stress-activated protein kinases (MSK) are epigenetic modifiers that regulate gene expression in normal and disease cell states. MSK1 and 2 are involved in a chain of signal transduction events bringing signals from the external environment of a cell to specific sites in the genome. MSK1/2 phosphorylate histone H3 at multiple sites, resulting in chromatin remodeling at regulatory elements of target genes and the induction of gene expression. Several transcription factors (RELA of NF-κB and CREB) are also phosphorylated by MSK1/2 and contribute to induction of gene expression. In response to signal transduction pathways, MSK1/2 can stimulate genes involved in cell proliferation, inflammation, innate immunity, neuronal function, and neoplastic transformation. Abrogation of the MSK-involved signaling pathway is among the mechanisms by which pathogenic bacteria subdue the host’s innate immunity. Depending on the signal transduction pathways in play and the MSK-targeted genes, MSK may promote or hinder metastasis. Thus, depending on the type of cancer and genes involved, MSK overexpression may be a good or poor prognostic factor. In this review, we focus on mechanisms by which MSK1/2 regulate gene expression, and recent studies on their roles in normal and diseased cells.
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-02-22T08:00:00Z
  DOI: 10.1139/bcb-2022-0371
Structural features, intrinsic disorder, and modularity of a pyriform
spidroin 1 core repetitive domain
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  Authors: Jeffrey R. Simmons, Geneviève Gasmi-Seabrook, Jan K. Rainey
  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  Orb-weaving spiders produce up to seven silk types, each with distinct biological roles, protein compositions, and mechanics. Pyriform (or piriform) silk is composed of pyriform spidroin 1 (PySp1) and is the fibrillar component of attachment discs that attach webs to substrates and to each other. Here, we characterize the 234-residue repeat unit (the “Py unit”) from the core repetitive domain of Argiope argentata PySp1. Solution-state nuclear magnetic resonance (NMR) spectroscopy-based backbone chemical shift and dynamics analysis demonstrate a structured core flanked by disordered tails, structuring that is maintained in a tandem protein of two connected Py units, indicative of structural modularity of the Py unit in the context of the repetitive domain. Notably, AlphaFold2 predicts the Py unit structure with low confidence, echoing low confidence and poor agreement to the NMR-derived structure for the Argiope trifasciata aciniform spidroin (AcSp1) repeat unit. Rational truncation, validated through NMR spectroscopy, provided a 144-residue construct retaining the Py unit core fold, enabling near-complete backbone and side chain 1H, 13C, and 15N resonance assignment. A six α-helix globular core is inferred, flanked by regions of intrinsic disorder that would link helical bundles in tandem repeat proteins in a beads-on-a-string architecture.
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-02-21T08:00:00Z
  DOI: 10.1139/bcb-2022-0338
ERCC6 plays a promoting role in the progression of non-small cell lung
cancer
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  Authors: Hui Luo, Zhehao Xiao, Cheng Huang, Wei Wu, Qingbin Xie
  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  Although excision repair cross-complementing group 6 (ERCC6) has been reported to be associated with lung cancer risk, the specific roles of ERCC6 in non-small cell lung cancer (NSCLC) progression are inadequately studied. Thus, this study aimed to examine the potential functions of ERCC6 in NSCLC. The expression of ERCC6 in NSCLC was analyzed by immunohistochemical staining and quantitative PCR. Celigo cell count, colony formation, flow cytometry, wound-healing, and transwell assays were used to evaluate the effects of ERCC6 knockdown on the proliferation, apoptosis, and migration of NSCLC cells. The effect of ERCC6 knockdown on tumor-forming ability of NSCLC cells was estimated by establishing xenograft model. ERCC6 was highly expressed in NSCLC tumor tissues and cell lines, and high ERCC6 expression was significantly associated with poor overall survival. Additionally, ERCC6 knockdown significantly suppressed cell proliferation, colony formation and migration, while accelerated cell apoptosis of NSCLC cells in vitro. Moreover, ERCC6 knockdown inhibited tumor growth in vivo. Further studies verified that ERCC6 knockdown attenuated the expression levels of Bcl-w, CCND1, and c-Myc. Altogether, these data unveil a major role of ERCC6 in the progression of NSCLC, and ERCC6 is expected to become a novel therapeutic target for NSCLC treatment.
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-02-21T08:00:00Z
  DOI: 10.1139/bcb-2022-0220
Lipid-induced alteration in retinoic acid signaling leads to mitochondrial
dysfunction in HepG2 and Huh7 cells
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  Authors: Eshani Karmakar, Nabanita Das, Bidisha Mukherjee, Prosenjit Das, Satinath Mukhopadhyay, Sib Sankar Roy
  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  A surfeit of mitochondrial reactive oxygen species (ROS) and inflammation serve as obligatory mediators of lipid-associated hepatocellular maladies. While retinoid homeostasis is essential in restoring systemic energy balance, its role in hepatic mitochondrial function remains elusive. The role of lecithin-retinol acyltransferase (LRAT) in maintenance of retinoid homeostasis is appreciated earlier; however, its role in modulating retinoic acid (RA) bioavailability upon lipid-imposition is unexplored. We identified LRAT overexpression in high-fat diet (HFD)-fed rats and palmitate-treated hepatoma cells. Elevation in LRAT expression depletes RA production and deregulates RA signaling. This altered RA metabolism enhances fat accumulation, accompanied by inflammation that leads to impaired mitochondrial function through enhanced ROS generation. Hence, LRAT inhibition could be a novel approach preventing lipid-induced mitochondrial dysfunction in hepatoma cells.
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-02-14T08:00:00Z
  DOI: 10.1139/bcb-2022-0266
GCN5 regulates ZBTB16 through acetylation, mediates osteogenic
differentiation, and affects orthodontic tooth movement
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  Authors: Shu-Man Shi, Ting-Ting Liu, Xue-Qin Wei, Ge-Hong Sun, Lin Yang, Juan-Fang Zhu
  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  In the process of orthodontic tooth movement (OTM), periodontal ligament fibroblasts (PDLFs) must undergo osteogenic differentiation. OTM increased the expression of Zinc finger and BTB domain-containing 16 (ZBTB16), which is implicated in osteogenic differentiation. Our goal was to investigate the mechanism of PDLF osteogenic differentiation mediated by ZBTB16. The OTM rat model was established, and PDLFs were isolated and exposed to mechanical force. Hematoxylin–eosin staining, Alizarin Red staining, immunofluorescence, and immunohistochemistry were carried out. The alkaline phosphatase (ALP) activity was measured. Dual-luciferase reporter gene assay and chromatin immunoprecipitation assay were conducted. In OTM models, ZBTB16 was significantly expressed. Additionally, there was an uneven distribution of PDLFs in the OTM group, as well as an increase in fibroblasts and inflammatory infiltration. ZBTB16 interference hindered PDLF osteogenic differentiation and decreased Wnt and β-catenin levels. Meanwhile, ZBTB16 activated the Wnt/β-catenin pathway. ZBTB16 also enhanced the expression of the osteogenic molecules osterix, osteocalcin (OCN), osteopontin (OPN), and bone sialo protein (BSP) at mRNA and protein levels. The interactions between Wnt1 and ZBTB16, as well as GCN5 and ZBTB16, were also verified. The adeno-associated virus-shZBTB16 injection also proved to inhibit osteogenic differentiation and reduce tooth movement distance in in vivo tests. ZBTB16 was up-regulated in OTM. Through acetylation modification of ZBTB16, GCN5 regulated the Wnt/β-catenin signaling pathway and further mediated PDLF osteogenic differentiation.
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-02-14T08:00:00Z
  DOI: 10.1139/bcb-2022-0080
Maternal use of methamphetamine alters cardiovascular function in the
adult offspring
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  Authors: Adam M. Belcher, Boyd R. Rorabaugh
  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  Methamphetamine is one of the most commonly used illicit drugs during pregnancy. Most studies investigating the impact of maternal use of methamphetamine on children have focused on neurological outcomes. In contrast, cardiovascular outcomes in these children have not been characterized. Recent studies in rodents provide evidence that prenatal exposure to methamphetamine induces changes in cardiac gene expression, changes in the heart's susceptibility to ischemic injury, and changes in vascular function that may increase the risk of developing cardiovascular disorders later in life. Importantly, these changes are sex-dependent. This review summarizes our current understanding of how methamphetamine use during pregnancy impacts the cardiovascular function of adult offspring and highlights gaps in our knowledge of the potential cardiovascular risks associated with prenatal exposure to methamphetamine.
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-02-10T08:00:00Z
  DOI: 10.1139/bcb-2022-0349
Epidermal melanocytes metabolize extracellular nucleotides by purinergic
enzymes
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  Authors: Liliana Ivet Sous Naasani, Jéssica Gonçalves Azevedo, Jean Sévigny, Tiago Franco de Oliveira, Silvya Stuchi Maria-Engler, Márcia Rosângela Wink
  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  The human epidermal melanocyte (hEM) are melanin-producing cells that provide skin pigmentation and protection against ultraviolet radiation. Although purinergic signaling is involved in skin biology and pathology, the presence of NTPDase members, as well as the rate of nucleotides degradation by melanocytes were not described yet. Therefore, in this study, we analyzed the expression of ectonucleotidases in hEM derived from discarded foreskin of male patients. The expression of purinergic enzymes was confirmed by mRNA and flow cytometry. Among the ectonucleotidases, ectonucleoside triphosphate diphosphohydrolase1 (NTPDase1) and ecto-5´-nucleotidase were the ectoenzymes with higher expressions. The hydrolysis rate for ATP, ADP, and AMP was low in comparison to other primary cells already investigated. The amount of ATP in the culture medium was increased after a scratch wound and decreased to basal levels in 48 h, while the NTPDase1 and P2X7 expressions increased. Therefore, it is possible to suggest that after cell injury, the ATP released by hEM into the extracellular space will be hydrolyzed by ectonucleotidases as the NTPDase1 that will control the levels of nucleotides in the skin micro-environment.
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-01-19T08:00:00Z
  DOI: 10.1139/bcb-2022-0058
RNA deadenylation complexes in development and diseases
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  Authors: Yilin Liu, Niveditha Ramkumar, Ly P. Vu
  First page: 131
  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  RNA deadenylation, the process of shortening of the 3′ poly(A) tail of an RNA molecule, is one of the key steps of post-transcriptional regulation of gene expression in eukaryotic cells. PAN2/3 and CCR4-NOT (CNOT) are the two dominant RNA deadenylation complexes, which play central roles in mediating mRNA decay and translation. While degradation is the final fate of virtually all RNAs in their life cycles, selection of RNA targets as well as control of the rate and timing of RNA decay, in coordination with other molecular pathways, including translation, can be modulated in certain contexts. Such regulation influences cell growth, proliferation, and differentiation at the cellular level; and contributes to establish polarity and regulate signaling at the tissue level. Dysregulation of deadenylation processes have also been implicated in human diseases ranging from cardiac diseases and neurodevelopmental disorders to cancers. In this review, we will discuss mechanisms of gene expression control mediated by the RNA deadenylation complexes and highlight relevant evidence supporting the emerging roles of RNA deadenylation and its regulatory proteins during development and in diseases. A systemic understanding of these mechanisms will be a critical foundation for development of effective strategies to therapeutically target them.
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-01-16T08:00:00Z
  DOI: 10.1139/bcb-2022-0325
The nuclear receptor subfamily 4 group A1 in human disease
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  Authors: Hongshuang Wang, Mengjuan Zhang, Fang Fang, Chang Xu, Jiazhi Liu, Lanjun Gao, Chenchen Zhao, Zheng Wang, Yan Zhong, Xiangting Wang
  First page: 148
  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  Nuclear receptor 4A1 (NR4A1), a member of the NR4A subfamily, acts as a gene regulator in a wide range of signaling pathways and responses to human diseases. Here, we provide a brief overview of the current functions of NR4A1 in human diseases and the factors involved in its function. A deeper understanding of these mechanisms can potentially improve drug development and disease therapy.
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-03-02T08:00:00Z
  DOI: 10.1139/bcb-2022-0331
Emerging roles for heterogeneous ribonuclear proteins in normal and
malignant B cells
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  Authors: Qurat Ul Ain Qureshi, Timothy E. Audas, Ryan D. Morin, Krysta M. Coyle
  First page: 160
  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  Heterogeneous nuclear ribonucleoproteins (hnRNPs) are among the most abundantly expressed RNA binding proteins in the cell and play major roles in all facets of RNA metabolism. hnRNPs are increasingly appreciated as essential for mammalian B cell development by regulating the carefully ordered expression of specific genes. Due to this tight regulation of the hnRNP-RNA network, it is no surprise that a growing number of genes encoding hnRNPs have been causally associated with the onset or progression of many cancers, including B cell neoplasms. Here we discuss our current understanding of hnRNP-driven regulation in normal, perturbed, and malignant B cells, and the most recent and emerging therapeutic innovations aimed at targeting the hnRNP–RNA network in lymphoma.
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-02-06T08:00:00Z
  DOI: 10.1139/bcb-2022-0332
Effects of the omega-3 fatty acid DHA on histone and p53 acetylation in
diffuse large B cell lymphoma
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  Authors: Tanner J. Bakhshi, Tanner Way, Bradley Muncy, Philippe T. Georgel
  First page: 172
  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  Diffuse large B cell lymphoma (DLBCL) often develops resistance and/or relapses in response to immunochemotherapy. Epigenetic modifiers are frequently mutated in DLBCL, i.e., the lysine (histone) acetyltransferases CREBBP and EP300. Mutations in CBP/p300 can prevent the proper acetylation and activation of (i) enhancer sequences of genes required for essential functions (e.g., germinal center exit and differentiation) and (ii) the tumor suppressor p53. Based on evidence that omega-3 fatty acids (ω-3 FAs) affect histone acetylation in various cancers, we investigated whether ω-3 FA docosahexaenoic acid (DHA) could modify levels of histone and p53 acetylation in three DLBCL cell lines (at different CREBBP/EP300 mutational status) versus normal B cells. Exposure to DHA at clinically attainable doses was shown to significantly alter the genome-wide levels of histone posttranslational modifications in a cell-line-dependent and dose-dependent manner. Although histone acetylation did not increase uniformly, as initially expected, levels of p53 acetylation increased consistently. Quantitative reverse transcription polymerase chain reaction results revealed significant changes in expression of multiple genes, including increased expression of CREBBP and of PRDM1 (required for differentiation into plasma cells or memory B cells). Taken together, our results provide (to our knowledge) the first characterization of the epigenetic effects of ω-3 FAs in DLBCL.
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-01-04T08:00:00Z
  DOI: 10.1139/bcb-2022-0288
Correction: Ultrasound-stimulated microbubbles contributes to radiotherapy
in esophageal carcinoma
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  Authors: Chenchun Fu, Jinjun Shi, Xiangyu Su, Shicheng Feng, Sheng Wang
  First page: 192
  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-02-14T08:00:00Z
  DOI: 10.1139/bcb-2022-0305
Retraction: MiR-154 inhibits the growth of laryngeal squamous cell
carcinoma by targeting GALNT7
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  First page: 197
  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  
  Citation: Biochemistry and Cell Biology
  PubDate: 2023-03-06T08:00:00Z
  DOI: 10.1139/bcb-2023-0037