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]

Proceedings of the Canadian Society for Molecular Biosciences (CSMB) 2024
Conference — Gene Regulation: From Cells to Systems
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  Authors: Mojgan Rastegar, Hans-Joachim Wieden, James R. Davie
  Pages: 1 - 3
  Abstract: Biochemistry and Cell Biology, Volume 103, Issue , Page 1-3, January 2025.
  The 67th Canadian Society for Molecular Biosciences (CSMB) Annual Conference took place in Winnipeg, Manitoba, from 6 May to 8 May 2024, at the University of Manitoba, Winnipeg. The conference theme “Gene Regulation: From Cells to Systems” was selected to reflect the breadth and multidisciplinary nature of CSMB's membership and to facilitate interactions among scientists and researchers across different disciplines and with diverse research programs and approaches. This meeting attracted registered participants from provinces across Canada and the USA. The objective of this meeting was to promote the inclusive dissemination, conversation, and discussions of molecular biosciences research, in different areas of molecular biosciences covering a wide range of topics in basic science and health-related research subjects such as neuroscience, cancer biology, immunology, physiology, bacterial systems, RNA biology, protein homeostasis, cellular metabolism and cell death mechanisms, neurobiology and neurogenetics, epigenetics, chromatin biology, environmental influence, stem cell biology, and genome-wide studies. This meeting provided a discussion opportunity for molecular bioscience researchers to develop innovative and novel strategies and collaborations for biomedical and translational research.
  Citation: Biochemistry and Cell Biology
  PubDate: 2025-06-17T07:00:00Z
  DOI: 10.1139/bcb-2025-0146
  Issue No: Vol. 103 (2025)
Revisiting galectin-1, -3, -4, and -9 as biotargets for colorectal cancer
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  Authors: Ammar Akram Kamarudin, Nadiah Abu
  Pages: 1 - 10
  Abstract: Biochemistry and Cell Biology, Volume 103, Issue , Page 1-10, January 2025.
  Galectins consist of a highly conserved carbohydrate recognition domain that involves in functional cellular activities including cell growth, cell proliferation and adhesion, signal transduction, and others. It has been reported that galectins play varying roles in distinct tissue types and have been implicated in different diseases, including cancer. Each of these proteins have its specific function and studies on the role of galectins in colorectal cancer mostly focusing on galectin-1, -3, -4, and -9. Thus, this review highlights the role of certain galectins in colorectal cancer, as well as their involvement in clinical trials.
  Citation: Biochemistry and Cell Biology
  PubDate: 2025-06-13T07:00:00Z
  DOI: 10.1139/bcb-2024-0218
  Issue No: Vol. 103 (2025)
Study on the mechanism of USP7 promoting endometriosis by regulating DNMT1
deubiquitination level
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  Authors: Xiangming Gao, Li Liu, Xueqin Liu, Yanru Shen, Yang Fan
  Pages: 1 - 14
  Abstract: Biochemistry and Cell Biology, Volume 103, Issue , Page 1-14, January 2025.
  Endometriosis is characterized by aberrant epigenetic regulation, and our study reveals that both Ubiquitin Specific Protease 7 (USP7) and DNA methyltransferase 1 (DNMT1) are significantly overexpressed in endometriosis tissues. Functional analyses in ectopic endometrial stromal cells (EESCs) indicate that elevated USP7 levels markedly enhance cellular proliferation, migration, and invasion, whereas silencing DNMT1 mitigates these oncogenic properties. Notably, USP7 and DNMT1 co-localize within the nucleus and interact directly, with USP7 modulating DNMT1 stability by attenuating its ubiquitination. The reduction in DNMT1 protein levels following USP7 silencing was reversed by proteasome inhibition, underscoring the pivotal role of USP7-mediated deubiquitination in maintaining DNMT1 stability. Furthermore, treatment with the USP7 inhibitor FT-671 significantly reduced DNMT1 protein expression while leaving its mRNA levels unaffected, and FT-671 effectively suppressed EESCs proliferation, migration, and invasion. Collectively, these findings suggest that USP7 contributes to the pathogenesis of endometriosis by sustaining DNMT1 expression and promoting aberrant cellular behaviors, thereby representing a promising therapeutic target for this disease.
  Citation: Biochemistry and Cell Biology
  PubDate: 2025-05-20T07:00:00Z
  DOI: 10.1139/bcb-2024-0301
  Issue No: Vol. 103 (2025)
Equity in action: a 4-year journey towards gender parity and racial
diversity in biochemistry hiring
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  Authors: Sherri L. Christian, Valerie Booth, Scott V Harding, Amy M. Todd, Mark D. Berry
  Pages: 1 - 9
  Abstract: Biochemistry and Cell Biology, Volume 103, Issue , Page 1-9, January 2025.
  Recruitment of faculty members in academic departments shapes the department for decades in research and teaching arenas. A diverse department is beneficial for all students as representation of underrepresented minority groups in the professoriate can inspire a greater diversity of students to pursue higher levels of education or research-focused careers. Increased diversity benefits research directly as diverse teams have been shown to have better ideas and outcomes. In 2020, our department had lower gender diversity than expected based on the pool of qualified personnel in Canada. Therefore, we altered our hiring process, primarily by redacting applications, for recruitment into entry-level tenure-track faculty positions. This resulted in the increased hiring of women (17% to 80%) with no substantial change in hiring of racially diverse individuals (50% to 40%). Overall, combined with retirements, the percentage of women faculty in the department went from 25% to 50% and the percentage of racialized faculty went from 38% to 44%. Thus, our intervention was successful in increasing the diversity of our department within a short timeframe. Our experience could provide other departments with a template for making substantive change, even in the absence of internal expertise in the area.
  Citation: Biochemistry and Cell Biology
  PubDate: 2025-05-20T07:00:00Z
  DOI: 10.1139/bcb-2025-0114
  Issue No: Vol. 103 (2025)
O-GlcNAcylation of epidermal growth factor receptor and glucose
transporter 1 prevents their intrinsic down regulation in breast cancer
cells
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  Authors: G. Pauline Padilla-Meier, Yeshika Bhatia, Suresh Mishra
  Pages: 1 - 13
  Abstract: Biochemistry and Cell Biology, Volume 103, Issue , Page 1-13, January 2025.
  The hexosamine biosynthetic pathway (HBP) is upregulated in many cancer cell types leading to upregulation of post-translational modification of proteins by β-N-acetylglucosamine (O-GlcNAc), the product of HBP. However, our knowledge of the identity of proteins that undergo O-GlcNAcylation in cancer cells and consequently their roles is very limited. We investigated the O-GlcNAcylation of epidermal growth factor receptor (EGFR) and glucose transporter 1 (GLUT1) in T47D and MDA-MB-231 breast cancer cell models. We examined the effect of the loss of putative O-GlcNAcylation sites in EGFR and GLUT1 on cell-signaling pathways and their functional consequences on cell cycle progression and cell metabolism using fluorescence-activated cell sorting analysis and in vitro assays. EGFR and GLUT1 undergo O-GlcNAcylation in T47D and MDA-MB-231 breast cancer cells, which enhances their functions and prevents their intrinsic downregulation. This appears to involve an interplay between phosphorylation, O-GlcNAcylation, and ubiquitination in both proteins. Importantly, perturbing the putative O-GlcNAcylation sites in both proteins adversely affected their stability, functions, and metabolic status of breast cancer cells, including glucose uptake and lactate production. In conclusion, the reprogrammed metabolism in cancer cells extends beyond energy and macromolecule requirements and contributes to cell-signaling events that support the stability and function of cancer promoting proteins.
  Citation: Biochemistry and Cell Biology
  PubDate: 2025-05-14T07:00:00Z
  DOI: 10.1139/bcb-2025-0055
  Issue No: Vol. 103 (2025)
Recombinant human holo-lactoferrin in complex with oleic acid suppresses
the growth of solid myeloma more efficiently than its apo-form
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  Authors: A. Yu. Elizarova, A.V. Sokolov, V.A. Kostevich, N.P. Gorbunov, I.V. Kudryavtsev, Yu. M. Berson, V.N. Yermalitsky, A.I. Budevich, V.B. Vasilyev
  Pages: 1 - 13
  Abstract: Biochemistry and Cell Biology, Volume 103, Issue , Page 1-13, January 2025.
  Our previous study showed antitumor activity of the complex formed by iron-free recombinant human lactoferrin (apo-recHLF) and oleic acid (OA) (1:8 molar ratio) in a model of murine hepatoma 22a inoculated to C3HA mice. Taken alone, apo-recHLF was less efficient; i.e., the tumor growth index was 0.14 for recHLF-8OA and 0.63 for recHLF as compared with 1.0 in the control animals. In the present study, we evaluated antitumor activity of iron-saturated recHLF per se and of the complexes formed by OA with apo-recHLF and holo-recHLF. Balb/c mice with solid myeloma Sp2/0 were subjected to the 10-day treatment with daily intraperitoneal (i/p) injections of 10 mg iron-saturated recHLF with OA (1:8) per animal (0.4 g/kg). In 15 days, the tumor growth was substantially inhibited. Mean tumor mass was 93% lower as compared with the control value (p
  Citation: Biochemistry and Cell Biology
  PubDate: 2025-04-26T07:00:00Z
  DOI: 10.1139/bcb-2024-0159
  Issue No: Vol. 103 (2025)
Lactoferrin enhances the antibiotic treatment of Staphylococcus aureus in
bone infection
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  Authors: Jillian Cornish, Reece Joseph, Jian-ming Lin, Stuart G. Irwin, Janesha Perera, Karen E. Callon, Jagir R. Hassan, Jingyuan Wen, Haemish Crawford, Brya G. Matthews, Nicholas N. Ashton, D. Williams, Heather M. Baker, Eduard N. Baker, Simon Swift
  Pages: 1 - 5
  Abstract: Biochemistry and Cell Biology, Volume 103, Issue , Page 1-5, January 2025.
  Lactoferrin (Lf), we have previously shown, has therapeutic potential in the field of skeletal regenerative medicine demonstrating its potent stimulating effects on bone growth. Recently, we have identified bovine lactoferrin (bLf) as a factor that also enhances antibiotic killing of Staphylococcus aureus (S. aureus). Biofilms are associated with around 65% of all infections and 80% of chronic infections. One feature of biofilm infection is tolerance to antibiotics due to the survival of a subpopulation of biofilm bacteria, where laboratory tests on planktonic cells indicate susceptibility. Tolerance is seen in bone infections of osteomyelitis and prosthetic joints, where methicillin-susceptible S. aureus (MSSA) strains predominate, but where treatments with the frontline penicillinase-resistant antibiotic cefazolin (CEF) can be ineffective. In vitro-grown biofilms of MSSA are 1000-fold more tolerant to CEF but can be eradicated by CEF at 10x minimal inhibitory concentration in the presence of bLf. Bone infection can impede blood circulation within the bone, leading to bone death. Lf as a potent stimulator of bone growth adds to its appeal as a treatment for bone infections.
  Citation: Biochemistry and Cell Biology
  PubDate: 2025-04-16T07:00:00Z
  DOI: 10.1139/bcb-2024-0101
  Issue No: Vol. 103 (2025)
Srcap loss alters H2A.Z-dependent and neuronal differentiation-related
gene expression in N2A cells
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  Authors: Karanveer S. Johal, Sandra A. Youssef, Samira M. Ibrahim, Lina A Dizon-Mapula, Isabella R. Galluzzo, Gilda Stefanelli
  Pages: 1 - 12
  Abstract: Biochemistry and Cell Biology, Volume 103, Issue , Page 1-12, January 2025.
  The chromatin remodeler SRCAP plays a critical role in depositing the histone variant H2A.Z, which is essential for transcriptional regulation, chromatin accessibility, and neurodevelopmental processes. Despite its known importance, the mechanisms by which SRCAP regulates H2A.Z dynamics during neuronal differentiation remain poorly understood. Here, we investigated the impact of Srcap knockdown on H2A.Z incorporation and transcriptional regulation in N2A cells. Chromatin immunoprecipitation revealed reduced H2A.Z occupancy at activity-dependent and neurodevelopmental genes upon Srcap knockdown, confirming Srcap’s role in H2A.Z deposition. Interestingly, CBP recruitment and global histone H3 acetylation were unaffected by Srcap knockdown at steady-state conditions, suggesting an H2A.Z-specific function of Srcap. We also observed that retinoic acid-induced neuronal differentiation leads to dynamic changes in H2A.Z levels at developmental loci, which are disrupted in Srcap-deficient cells. Gene expression analysis revealed altered expression of neurodevelopmental genes in the absence of Srcap, correlating with reduced H2A.Z occupancy. Together, these findings demonstrate that Srcap is essential for regulating H2A.Z dynamics and gene expression during neuronal differentiation, offering new insights into its role in chromatin remodelling and its potential involvement in neurodevelopmental disorders.
  Citation: Biochemistry and Cell Biology
  PubDate: 2025-04-10T07:00:00Z
  DOI: 10.1139/bcb-2024-0294
  Issue No: Vol. 103 (2025)
Lysosomal enzyme processing and trafficking in the social amoeba
Dictyostelium discoideum
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  Authors: Sean V. Condie, William D. Kim, Robert J. Huber
  Pages: 1 - 11
  Abstract: Biochemistry and Cell Biology, Volume 103, Issue , Page 1-11, January 2025.
  Dictyostelium discoideum is a single-celled protist that undergoes multicellular development in response to nutrient deprivation. For close to a century, D. discoideum has been used as a model system for studying conserved cellular and developmental processes such as chemotaxis, cell adhesion, and cell differentiation. In the later decades of the 20th century, intensive research efforts examined the synthesis, trafficking, and activity of lysosomal enzymes in D. discoideum. Subsequent work revealed that lysosomes are essential for all stages of the D. discoideum life cycle and the genome encodes dozens of homologs of human lysosomal enzymes, including those associated with lysosomal storage diseases. Additionally, protocols for examining the trafficking and activity of lysosomal enzymes in D. discoideum are well-established. Here, we provide a comprehensive up-to-date review that summarizes our current knowledge of lysosomal enzyme processing and trafficking in D. discoideum, with an eye towards re-establishing D. discoideum as a model eukaryote for studying the functions of conserved lysosomal enzymes and the pathways that regulate their trafficking.
  Citation: Biochemistry and Cell Biology
  PubDate: 2025-04-01T07:00:00Z
  DOI: 10.1139/bcb-2025-0062
  Issue No: Vol. 103 (2025)
Establishment of immortalized porcine intramuscular preadipocytes for the
study of lipid metabolism
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  Authors: Briana Locke, Ray Lu
  Pages: 1 - 11
  Abstract: Biochemistry and Cell Biology, Volume 103, Issue , Page 1-11, January 2025.
  Intramuscular adipose tissue is associated with an increased risk for the development of metabolic syndrome. A cellular model of adipogenesis in muscular tissues would be an invaluable tool for studying regulatory factors in this important process. Cellular stress can impact the homeostasis of various metabolic pathways, including lipid metabolism. In this study, a porcine intramuscular preadipocyte cell line was established, which displayed mature adipocyte attributes such as lipid accumulation and increased expression of adipogenic gene markers. Since it is well established that endoplasmic reticulum (ER) and Golgi stress impact adipogenesis, we sought to investigate the effects of ER/Golgi stress and an associated protein, CREB3, in this cell line model. We found that this novel model maintains robust adipogenic capabilities, and that ER stress can negatively affect adipogenic markers. Overall, these findings demonstrate the strength of the new cell model for studying adipogenesis, and highlight the impact of ER stress on lipid metabolism.
  Citation: Biochemistry and Cell Biology
  PubDate: 2025-03-24T07:00:00Z
  DOI: 10.1139/bcb-2024-0174
  Issue No: Vol. 103 (2025)
Effects of different sources of lactoferrin on cytokine response to
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  Authors: Rulan Jiang, Xiaogu Du, Bo Lönnerdal
  Pages: 1 - 12
  Abstract: Biochemistry and Cell Biology, Volume 103, Issue , Page 1-12, January 2025.
  Lactoferrin (Lf) is a multifunctional iron-binding glycoprotein, involved in a wide range of bioactivities, including immunomodulatory and antiviral activities. Lf in human milk and bovine Lf added to infant formula may provide some protection against viral infections. However, functions of Lfs from different sources may differ due to varying manufacturing processes and posttranslational modifications. Here, effects of Lfs (11 commercial bovine milk Lfs, 2 recombinant Lfs, and native human/bovine milk Lf) on cytokine responses to virus infection were examined by infecting human intestinal epithelial cells (Caco-2 cells) with rotavirus (naked) or normal human bronchial epithelial cells (BEAS-2B cells) with respiratory syncytial virus (RSV, enveloped) or severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike protein 1. Effects of Lf on viral infection were evaluated by quantitative real-time polymerase chain reaction analysis of transcripts of cytokines/chemokines (TNF-α, IL-1β, IL-6, IL-8, IL-10, IFN-β, and CXCL10). Our results show that viral infection changes transcription of these cytokines and that Lfs significantly and variously influence immune responses to rotavirus, RSV, and SARS-CoV-2 in vitro. Thus, Lf may provide protection against virus infection by down-regulating pro–inflammatory cytokine/chemokine responses. Recombinant bovine and human Lf show similar effects as bovine milk Lfs suggesting that different posttranslational modifications do not affect the antiviral activity on cytokine response.
  Citation: Biochemistry and Cell Biology
  PubDate: 2025-03-14T07:00:00Z
  DOI: 10.1139/bcb-2024-0146
  Issue No: Vol. 103 (2025)
Retraction: The mechanism behind BAF60c in myocardial metabolism in rats
with heart failure is through the PGC1α-PPARα-mTOR signaling pathway
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  Pages: 1 - 1
  Abstract: Biochemistry and Cell Biology, Volume 103, Issue , Page 1-1, January 2025.
  
  Citation: Biochemistry and Cell Biology
  PubDate: 2025-02-28T08:00:00Z
  DOI: 10.1139/bcb-2025-0023
  Issue No: Vol. 103 (2025)
Retraction: PYGB facilitates cell proliferation and invasiveness in
non-small cell lung cancer by activating the Wnt–β-catenin signaling
pathway
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  Pages: 1 - 1
  Abstract: Biochemistry and Cell Biology, Volume 103, Issue , Page 1-1, January 2025.
  
  Citation: Biochemistry and Cell Biology
  PubDate: 2025-02-28T08:00:00Z
  DOI: 10.1139/bcb-2025-0022
  Issue No: Vol. 103 (2025)
Retraction: MiR-1180 promotes cardiomyocyte cell cycle re-entry after
injury through the NKIRAS2–NFκB pathway
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  Pages: 1 - 1
  Abstract: Biochemistry and Cell Biology, Volume 103, Issue , Page 1-1, January 2025.
  
  Citation: Biochemistry and Cell Biology
  PubDate: 2025-02-28T08:00:00Z
  DOI: 10.1139/bcb-2025-0052
  Issue No: Vol. 103 (2025)
A role for NFIB in SOX2 downregulation and epigenome accessibility changes
due to long-term estrogen treatment of breast cancer epithelial cells
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  Authors: Luis E. Abatti, Zoe E. Gillespie, Patricia Lado-Fernández, Manuel Collado, Jennifer A. Mitchell
  Pages: 1 - 14
  Abstract: Biochemistry and Cell Biology, Volume 103, Issue , Page 1-14, January 2025.
  Estrogen (E2) regulates the differentiation and proliferation of mammary progenitor cells by modulating the transcription of multiple genes. One of the genes that is downregulated by E2 is SOX2, a transcription factor associated with stem and progenitor cells that is overexpressed during breast tumourigenesis. To elucidate the mechanisms underlying E2-mediated SOX2 repression, we investigated epigenome and transcriptome changes following short- and long-term E2 exposure in breast cancer cells. We found that short-term E2 exposure reduces chromatin accessibility at the downstream SOX2 SRR134 enhancer, decreasing SOX2 expression. In contrast, long-term E2 exposure completely represses SOX2 transcription while maintaining accessibility at the SRR124–134 enhancer cluster, keeping it poised for reactivation. This repression was accompanied by widespread epigenome and transcriptome changes associated with commitment towards a more differentiated and less invasive luminal phenotype. Finally, we identified a role for the transcription factor NFIB in this process, suggesting it collaborates with the estrogen receptor to mediate SOX2 repression and genome-wide epigenome accessibility changes.
  Citation: Biochemistry and Cell Biology
  PubDate: 2025-02-26T08:00:00Z
  DOI: 10.1139/bcb-2024-0287
  Issue No: Vol. 103 (2025)
WDR4 promotes colorectal cancer progression by activating the
GSK3β/β-catenin pathway
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  Authors: Hongyu Wang, Liyang Liang, Yanfei Wang, Xuan Zhong, Chao Zhang, Zhipeng Liu, Jinzhong Liu, Wanning Hu
  Pages: 1 - 12
  Abstract: Biochemistry and Cell Biology, Volume 103, Issue , Page 1-12, January 2025.
  WD repeat domain 4 (WDR4) has been reported to promote tumor metastasis in various cancers. However, its precise function in colorectal cancer (CRC) has not been reported yet. Herein, the expression pattern of WDR4 in CRC was determined by analyzing Gene Expression Omnibus datasets (GSE110225, GSE127069, GSE156355, and GSE184093) and GEPIA online dataset. In vitro and in vivo experiments, including CCK-8, colony formation, flow cytometry, wound healing, transwell assays, and xenograft mouse models, were used to investigate the role of WDR4 in CRC. Firstly, data from Kaplan–Meier database showed that high expression of WDR4 was associated with the poor prognosis of CRC patients. Then, upregulation of WDR4 was confirmed in clinical CRC tissues. In vitro functional experiments suggested that overexpression of WDR4 promoted cell proliferation, migration, and invasion, while knockdown of WDR4 has the opposite effects. Also, the oncogenic role of WDR4 was also verified in in vivo experiments. CO-IP-LC/MS analysis uncovered that glycogen synthase kinase 3β (GSK3β) is the central protein that binds to WDR4. Mechanistically, WDR4 activated the β-catenin pathway by promoting GSK3β phosphorylation. This study demonstrates that WDR4 promotes CRC progression through activating GSK3β/β-catenin pathway, indicating that WDR4 might be a potential therapeutic target for CRC treatment.
  Citation: Biochemistry and Cell Biology
  PubDate: 2025-02-26T08:00:00Z
  DOI: 10.1139/bcb-2024-0168
  Issue No: Vol. 103 (2025)
Retraction: Long noncoding RNA HIF1A-AS2 facilitates cell survival and
migration by sponging miR-33b-5p to modulate SIRT6 expression in
osteosarcoma
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  Pages: 1 - 1
  Abstract: Biochemistry and Cell Biology, Volume 103, Issue , Page 1-1, January 2025.
  
  Citation: Biochemistry and Cell Biology
  PubDate: 2025-02-26T08:00:00Z
  DOI: 10.1139/bcb-2025-0019
  Issue No: Vol. 103 (2025)
Retraction: LncRNA MALAT1 regulates diabetic cardiac fibroblasts through
the Hippo–YAP signaling pathway
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  Pages: 1 - 1
  Abstract: Biochemistry and Cell Biology, Volume 103, Issue , Page 1-1, January 2025.
  
  Citation: Biochemistry and Cell Biology
  PubDate: 2025-02-26T08:00:00Z
  DOI: 10.1139/bcb-2025-0021
  Issue No: Vol. 103 (2025)
Retraction: MicroRNA-24 alleviates isoflurane-induced neurotoxicity in rat
hippocampus via attenuation of oxidative stress
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  Pages: 1 - 1
  Abstract: Biochemistry and Cell Biology, Volume 103, Issue , Page 1-1, January 2025.
  
  Citation: Biochemistry and Cell Biology
  PubDate: 2025-02-26T08:00:00Z
  DOI: 10.1139/bcb-2025-0018
  Issue No: Vol. 103 (2025)
Retraction: Active vitamin D activates chondrocyte autophagy to reduce
osteoarthritis via mediating the AMPK–mTOR signaling pathway
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  Pages: 1 - 1
  Abstract: Biochemistry and Cell Biology, Volume 103, Issue , Page 1-1, January 2025.
  
  Citation: Biochemistry and Cell Biology
  PubDate: 2025-02-26T08:00:00Z
  DOI: 10.1139/bcb-2025-0020
  Issue No: Vol. 103 (2025)
Doxorubicin, a DNA intercalator, inhibits transcription elongation
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  Authors: Mathew Tempel, Kari Green, Dhanvi Prajapati, Angela Duaqui, Mahboobeh Norouzi, Hedieh Sattarifard, Ahmed Ashraf, Elly Wu, Athanasios Zovoilis, Ted M. Lakowski, James R. Davie
  Pages: 1 - 12
  Abstract: Biochemistry and Cell Biology, Volume 103, Issue , Page 1-12, January 2025.
  Doxorubicin is a chemotherapeutic drug for cancer that intercalates into nucleosome-free regions at promoters. Doxorubicin was reported to result in loss of histone H3 trimethylated lysine 4 (H3K4me3). To further explore doxorubicin’s mechanism of action, we determined the genomic location of the binding sites of doxorubicin in leukemic cells. The effect of doxorubicin intercalation into the chromatin of leukemic cells on histone modifications was also determined. We show that doxorubicin binding sites were present in the nucleosome-free regions associated with regulatory regions (promoters, enhancers, and super-enhancers) and in the gene body (introns). Doxorubicin treatment did not alter the levels of H3K4me3 and many other histone modifications but significantly lowered H2B ubiquitinated at lysine 120 (H2BK120ub), an elongation-dependent modification. Lastly, we demonstrate that doxorubicin results in the degradation of the largest subunit (RPB1) of RNA polymerase II.
  Citation: Biochemistry and Cell Biology
  PubDate: 2025-02-14T08:00:00Z
  DOI: 10.1139/bcb-2024-0264
  Issue No: Vol. 103 (2025)
Omega-3 polyunsaturated fatty acids modify glucose metabolism in THP-1
monocytes
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  Authors: Michael J. Byun, Roni Armon, Tamiris F.G. Souza, Hope D. Anderson, Ayesha Saleem, Samantha D. Pauls
  Pages: 1 - 10
  Abstract: Biochemistry and Cell Biology, Volume 103, Issue , Page 1-10, January 2025.
  Chronic inflammation is a driving factor in diseases like obesity and type 2 diabetes. Enhanced cellular glucose metabolism may contribute to heightened immune activation. A human supplementation trial showed that the n-3 PUFA α-linolenic acid (ALA) reduced oxidative phosphorylation in monocytes. Our objective here is to assess the direct effects of ALA and docosahexaenoic acid (DHA) on glucose metabolism in a cell culture model and to explore possible molecular mechanisms. THP-1 monocytes were treated with 10–40 µmol/L of ALA or DHA and compared with vehicle and oleic acid controls. The Seahorse XFe24 and Oroboros O2k Oxygraph systems were used to approximate catabolic rates in the presence of glucose. Both ALA and DHA reduced oxidative phosphorylation. We identified pyruvate dehydrogenase kinase 4 (PDK4) as a possible mechanistic candidate explaining the effect of DHA. Additionally, both n-3 PUFAs reduced lipopolysaccharides-induced IL-1β production, while only DHA increased reactive oxygen species to a small but significant extent. Our data suggest that ALA and DHA trigger a re-wiring of bioenergetic pathways in monocytes, possibly via the upregulation of PDK4. Given the close relationship between cell metabolism and immune cell activation, this may represent a novel mechanism by which n-3 fatty acids modulate immune function and inflammation.
  Citation: Biochemistry and Cell Biology
  PubDate: 2025-02-03T08:00:00Z
  DOI: 10.1139/bcb-2024-0202
  Issue No: Vol. 103 (2025)
A novel mouse model of pulmonary fibrosis: twice-repeated oropharyngeal
bleomycin administration mimicking human pathology
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  Authors: Jingyu Wang, Fengqing Zhu, Yuxuan Liu, Renru Luo, Zixuan Fan, Wanqin Dai, Shuquan Wei, Chuwen Lin
  Pages: 1 - 7
  Abstract: Biochemistry and Cell Biology, Volume 103, Issue , Page 1-7, January 2025.
  Idiopathic pulmonary fibrosis (IPF) is a progressive and irreversible lung disease with high mortality and limited treatment options. While single-dose bleomycin-induced models are commonly used to investigate the pathogenesis of IPF, they fail to adequately replicate the complex pathological features in human patients, thereby hindering comprehensive investigations. Previous studies utilizing repetitive bleomycin injections have demonstrated a closer resemblance to human IPF pathology; however, the time- and resource-intensive nature of this approach presents significant drawbacks. Here, we propose a novel methodology involving twice-repeated oropharyngeal administration of bleomycin in mice, which closely mirrors the pathological manifestations observed in IPF patients. This model exhibited the honeycomb-like cyst formation, fibroblastic foci, bronchiolization of alveolar epithelium, emergence of metaplastic alveolar KRT5+ basal cells, and sustainability of these fibrotic phenotypes, thereby providing a robust model for IPF. Our findings establish a more efficient and translatable preclinical platform for investigating IPF pathogenesis and exploring potential therapeutic strategies.
  Citation: Biochemistry and Cell Biology
  PubDate: 2025-01-29T08:00:00Z
  DOI: 10.1139/bcb-2024-0221
  Issue No: Vol. 103 (2025)
Efficacy of lactoferrin supplementation in pediatric infections: a
systematic review and meta-analysis
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  Authors: Valerie S. Mayorga, Rafaella Navarro, Victor D. Torres Roldan, Meritxell Urtecho, Silvia Tipe, Bea Calvert, Laura A. Wright, Theresa J. Ochoa
  Pages: 1 - 23
  Abstract: Biochemistry and Cell Biology, Volume 103, Issue , Page 1-23, January 2025.
  Pediatric infections account for approximately one-third of all deaths in children under 5 years globally. Lactoferrin (LF) supplementation has the potential to reduce infection-related morbidity due to its antimicrobial, anti-inflammatory, and immunoregulatory properties. We conducted a systematic review and meta-analysis of oral LF supplementation randomized controlled trials in population under 18 years old. The primary outcomes were infection-associated outcomes: late onset sepsis (LOS), diarrhea, and upper respiratory infections (URIs). We also analyzed mortality among LOS studies. Of 1594 citations identified, 25 studies met eligibility criteria, including 10 studies of LOS, 14 of diarrhea, and 8 of URI. LF supplementation was associated with fewer patients with culture-proven or probable neonatal LOS compared to placebo (odds ratio (OR): 0.60; 95% confidence interval (CI): 0.42–0.86), with fewer patients with diarrhea compared to placebo in children (OR: 0.56; 95% CI: 0.41–0.75), and no significant fewer patients with URI (OR: 0.61; 95% CI: 0.27–1.40). Before LF can be used as a public health intervention, it is necessary to refine some aspects of the design of future trials. Ideally these trials should be conducted in countries with the highest burden of infections, where the potential benefit is expected to have the largest impact.
  Citation: Biochemistry and Cell Biology
  PubDate: 2025-01-22T08:00:00Z
  DOI: 10.1139/bcb-2024-0181
  Issue No: Vol. 103 (2025)
Note of appreciation
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  Pages: 1 - 1
  Abstract: Biochemistry and Cell Biology, Volume 103, Issue , Page 1-1, January 2025.
  
  Citation: Biochemistry and Cell Biology
  PubDate: 2025-01-10T08:00:00Z
  DOI: 10.1139/bcb-2024-0284
  Issue No: Vol. 103 (2025)
Multifaceted roles of MeCP2 in cellular regulation and phase separation:
implications for neurodevelopmental disorders, depression, and oxidative
stress
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  Authors: Katrina V. Good, Ladan Kalani, John B. Vincent, Juan Ausió
  Pages: 1 - 12
  Abstract: Biochemistry and Cell Biology, Volume 103, Issue , Page 1-12, January 2025.
  Methyl CpG binding protein 2 (MeCP2) is a chromatin-associated protein that remains enigmatic despite more than 30 years of research, primarily due to the ever-growing list of its molecular functions, and, consequently, its related pathologies. Loss of function MECP2 mutations cause the neurodevelopmental disorder Rett syndrome (RTT); in addition, dysregulation of MeCP2 expression and/ or function are involved in numerous other pathologies, but the mechanisms of MeCP2 regulation are unclear. Advancing technologies and burgeoning mechanistic theories assist our understanding of the complexity of MeCP2 but may inadvertently cloud it if not rigorously tested. Here, rather than focus on RTT, we examine relatively underexplored aspects of MeCP2, such as its dosage homeostasis at the gene and protein levels, its controversial participation in phase separation, and its overlooked role in depression and oxidative stress. All these factors may be essential to understanding the full scope of MeCP2 function in healthy and diseased states, but are relatively infrequently studied and require further criticism. The aim of this review is to discuss the esoteric facets of MeCP2 at the molecular and pathological levels and to consider to what extent they may be necessary for general MeCP2 function.
  Citation: Biochemistry and Cell Biology
  PubDate: 2025-01-06T08:00:00Z
  DOI: 10.1139/bcb-2024-0237
  Issue No: Vol. 103 (2025)
How prevalent are lactoferrin receptors in Gram-negative bacteria'
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  Authors: Nikolas F. Ewasechko, David M. Curran, Ken Yu Khaw, Anthony B. Schryvers
  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  Surface receptors in Gram-negative bacteria that bind and extract iron from the host glycoproteins transferrin (Tf) or lactoferrin (Lf) was discovered 35 years ago in pathogenic Neisseria species and subsequently was discovered in other pathogens of humans and food production animals. These bacterial species reside exclusively on the mucosal surfaces of the respiratory or genitourinary tract of their mammalian host and rely on their host specific Tf and Lf receptors to acquire iron for survival. Since the specificity of the bacterial Tf receptors was shown to be due to selective pressures on the host Tf, their presence in bacteria that reside in both mammals and birds indicates that they arose over 320 million years ago. Once Lf arose in mammals due to a gene duplication event, Lf receptors subsequently arose from Tf receptors. The focus on pathogens for discovery of these receptors has led to a limited understanding of how prevalent the Tf and Lf receptors are in commensal species and raises the question whether they are present in additional bacterial lineages. Since the Lf receptor provides a secondary iron acquisition system plus can provide protection from cationic peptides its presence varies in bacterial lineages.
  Citation: Biochemistry and Cell Biology
  PubDate: 2025-01-09T08:00:00Z
  DOI: 10.1139/bcb-2024-0180
LMAN2 interacts with HEATR3 to expedite HER2-positive breast cancer
advancement and inflammation and Akt/ERK/NF-κB signaling
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  Authors: Sujian Xiao, Tong Yu, Fulan Yang, Huozhong Yuan, Jun Ni
  Abstract: Biochemistry and Cell Biology, Ahead of Print.
  The paper aimed to reveal the impacts and the possible mechanism of action of lectin mannose-binding 2 protein (LMAN2) in HER2-positive breast cancer (BC). The expression, prognostic potential of LMAN2, and the correlation between LMAN2 and HEAT repeat containing 3 (HEATR3) in BC were analyzed in TCGA database. Intact, Mentha, and BioGrid databases predicted LMAN2–HEATR3 interactions. Reverse transcription-quantitative PCR and Western blot examined LMAN2 expression. Cell Counting Kit-8, 5-ethynyl-2′-deoxyuridine staining, wound healing, and transwell assays, respectively, detected the aggressive cellular biological behaviors including proliferation, migration, and invasion. Western blot analyzed the expression of matrix metalloproteinases, HEATR3, and protein kinase B (Akt)/extracellular signal-regulated kinase (ERK)/nuclear factor-kappaB (NF-κB) signaling-related proteins. Co-immunoprecipitation assay was used to prove the relationship of LMAN2 with HEATR3. Enzyme-linked immunosorbent assay detected inflammatory cytokine levels. LMAN2 was overexpressed in HER2-positive BC tissues and cells and indicated unfavorable prognosis of BC patients. LMAN2 knockdown suppressed HER2-positive BC cell proliferation, migration, and invasion. LMAN2 interacted with and had a positive correlation with HEATR3. HEATR3 up-regulation reversed the repressive role of LMAN2 interference in the progression of HER2-positive BC, Akt/ERK/NF-κB signaling, and inflammatory response. Altogether, LMAN2 silencing might exert anti-tumor and anti-inflammatory properties and inactivate Akt/ERK/NF-κB signaling in HER2-positive BC via binding to HEATR3.
  Citation: Biochemistry and Cell Biology
  PubDate: 2025-01-08T08:00:00Z
  DOI: 10.1139/bcb-2024-0166

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