Biochemistry and Cell Biology最新文献

A role for NFIB in SOX2 downregulation and epigenome accessibility changes due to long-term estrogen treatment of breast cancer epithelial cells.

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-02-26 DOI: 10.1139/bcb-2024-0287

Luis E Abatti, Zoe E Gillespie, Patricia Lado-Fernández, Manuel Collado, Jennifer A Mitchell

{"title":"A role for NFIB in SOX2 downregulation and epigenome accessibility changes due to long-term estrogen treatment of breast cancer epithelial cells.","authors":"Luis E Abatti, Zoe E Gillespie, Patricia Lado-Fernández, Manuel Collado, Jennifer A Mitchell","doi":"10.1139/bcb-2024-0287","DOIUrl":"https://doi.org/10.1139/bcb-2024-0287","url":null,"abstract":"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.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

WDR4 promotes colorectal cancer progression by activating the GSK3β/β-catenin pathway.

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-02-26 DOI: 10.1139/bcb-2024-0168

Hongyu Wang, Liyang Liang, Yanfei Wang, Xuan Zhong, Chao Zhang, Zhipeng Liu, Jinzhong Liu, Wanning Hu

{"title":"WDR4 promotes colorectal cancer progression by activating the GSK3β/β-catenin pathway.","authors":"Hongyu Wang, Liyang Liang, Yanfei Wang, Xuan Zhong, Chao Zhang, Zhipeng Liu, Jinzhong Liu, Wanning Hu","doi":"10.1139/bcb-2024-0168","DOIUrl":"https://doi.org/10.1139/bcb-2024-0168","url":null,"abstract":"WD repeat domain 4 (WDR4) has been reported to promote tumor metastasis in various cancers. However, its precise function in colorectal cancer (CRC) have not been reported yet. Herein, the expression pattern of WDR4 in CRC were 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 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.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Doxorubicin, a DNA intercalator, inhibits transcription elongation.

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-02-14 DOI: 10.1139/bcb-2024-0264

Mathew Tempel, Kari Green, Dhanvi Prajapati, Angela Duaqui, Mahboobeh Norouzi, Hedieh Sattarifard, Ahmed Ashraf, Elly Wu, Athanasios Zovoilis, Ted M Lakowski, James R Davie

引用次数: 0

Omega-3 polyunsaturated fatty acids modify glucose metabolism in THP-1 monocytes.

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-02-03 DOI: 10.1139/bcb-2024-0202

Michael Jae-Ho Byun, Roni Armon, Tamiris F G Souza, Hope D Anderson, Ayesha Saleem, Samantha Dawn Pauls

{"title":"Omega-3 polyunsaturated fatty acids modify glucose metabolism in THP-1 monocytes.","authors":"Michael Jae-Ho Byun, Roni Armon, Tamiris F G Souza, Hope D Anderson, Ayesha Saleem, Samantha Dawn Pauls","doi":"10.1139/bcb-2024-0202","DOIUrl":"https://doi.org/10.1139/bcb-2024-0202","url":null,"abstract":"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 mechanisms. THP-1 monocytes were treated with 10-40 μM 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 LPS-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 PKD4. Given the close relationship between cell metabolism and immune cell activation, this may represent a novel mechanism by which n-3 PUFAs modulate immune function and inflammation.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143121857","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Efficacy of lactoferrin supplementation in pediatric infections: A systematic review and meta-analysis.

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-22 DOI: 10.1139/bcb-2024-0181

Valerie S Mayorga, Rafaella Navarro, Victor D Torres Roldan, Meritxell Urtecho, Silvia Tipe, Bea Calvert, Laura A Wright, Theresa J Ochoa

{"title":"Efficacy of lactoferrin supplementation in pediatric infections: A systematic review and meta-analysis.","authors":"Valerie S Mayorga, Rafaella Navarro, Victor D Torres Roldan, Meritxell Urtecho, Silvia Tipe, Bea Calvert, Laura A Wright, Theresa J Ochoa","doi":"10.1139/bcb-2024-0181","DOIUrl":"https://doi.org/10.1139/bcb-2024-0181","url":null,"abstract":"Pediatric infections account for approximately one-third of all deaths in children under 5 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 (RCT) in population under 18 years old. The primary outcomes were infection-associated outcomes: late onset sepsis (LOS), diarrhea, and upper respiratory infections (URI). We also analyzed mortality among LOS studies. Of 1,594 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 (OR: 0.60; 95% CI: 0.42 to 0.86), with fewer patients with diarrhea compared to placebo in children (OR: 0.56; 95% CI: 0.41 to 0.75), and no significant fewer patients with URI (OR: 0.61; 95% CI: 0.27 to 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.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143021954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Origin of dedifferentiated adipocyte-derived cells (DFAT) during ceiling culture in an Adiponectin Cre-Recombinase mouse model. 在脂肪蛋白 Cre 重组酶小鼠模型的上限培养过程中，已分化脂肪细胞衍生细胞（DFAT）的起源。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 Epub Date: 2024-10-30 DOI: 10.1139/bcb-2024-0140

Marie-Frédérique Gauthier, Giada Ostinelli, Mélissa Pelletier, André Tchernof

{"title":"Origin of dedifferentiated adipocyte-derived cells (DFAT) during ceiling culture in an Adiponectin Cre-Recombinase mouse model.","authors":"Marie-Frédérique Gauthier, Giada Ostinelli, Mélissa Pelletier, André Tchernof","doi":"10.1139/bcb-2024-0140","DOIUrl":"10.1139/bcb-2024-0140","url":null,"abstract":"DFAT cells represent an attractive source of stem cells in tissue engineering and in the potential treatment of several clinical conditions. Our objective was to determine whether DFAT cells originate from mature adipocytes and address whether contamination from the stromal vascular fraction (SVF) could be as a source for these cells. A murine adiponectin-creERT;mT/mG model was used with the excision of the cassette induced by tamoxifen injection for the cells expressing adiponectin (adipoq). This model allows distinguishing of mature adipocytes (green fluorescence) from other SVF cell types (red fluorescence) based on the fluorescent protein expressed. Mature adipocytes and SVF cells were isolated from adipose tissues by collagenase digestion. Ceiling cultures were imaged by time-lapse microscopy. Confocal microscopy was used to follow cells over 21 days. Time-lapse microscopy experiments showed liposecretion occurring in mature adipocytes displaying green fluorescence. Confocal imaging allowed the identification of a heterogeneous cell population expressing green but also red fluorescence after 21 days of culture. Asymmetrical division of mature adipocytes was not observed. In conclusion, liposecretion of mature adipocytes is a phenomenon that can be observed in vitro and DFAT cells do originate from mature adipocytes. However, the population of DFAT cells is heterogenous.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-10"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142543388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

1-Deoxynojirimycin affects high glucose-induced pancreatic beta-cell dysfunction through regulating CEBPA expression and AMPK pathway. 1-脱氧野尻霉素通过调节CEBPA表达和AMPK通路影响高血糖诱导的胰岛β细胞功能障碍

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 Epub Date: 2024-11-15 DOI: 10.1139/bcb-2024-0128

Xiaoying Li, Shenggui Liu, Siqi Wang, Xinghui Ai, Lin Wei

引用次数: 0

TRIM3 modulates cisplmatin-resistant of cervical squamous cell carcinoma via endoplasmic reticulum stress signaling in vitro. TRIM3在体外通过内质网应激信号调节宫颈鳞癌顺铂耐药。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 Epub Date: 2024-12-02 DOI: 10.1139/bcb-2024-0154

Meiya Mao, Tianzi You, Kejun Xu, Huiqing Ding

{"title":"TRIM3 modulates cisplmatin-resistant of cervical squamous cell carcinoma via endoplasmic reticulum stress signaling in vitro.","authors":"Meiya Mao, Tianzi You, Kejun Xu, Huiqing Ding","doi":"10.1139/bcb-2024-0154","DOIUrl":"10.1139/bcb-2024-0154","url":null,"abstract":"TRIM3 is widely recognized as a tumor suppressor gene. However, its precise role in cervical squamous cell carcinoma (CESC) remains elusive. Here, we observed a significant decrease in the expression of TRIM3 in CESC cells. Overexpression of TRIM3 suppresses cell proliferation and clonal formation. Through the establishment of cisplatin (cDDP)-resistant CESC cell lines, we discovered that the expression of TRIM3 was further downregulated in cDDP-resistant cells, while overexpression of TRIM3 enhanced cellular sensitivity to cDDP. Mechanistic investigations revealed that TRIM3 directly interacts with GRP78, a crucial protein involved in endoplasmic reticulum stress (ERS) pathway, promoting its ubiquitination degradation. Under cDDP treatment, the overexpression of TRIM3 in cDDP-resistant cells suppressed cell proliferation and downregulated the expression of drug-resistant genes, while simultaneously enhancing the activation of apoptosis signaling pathways. However, co-expression of TRIM3 and GRP78 restored cellular sensitivity to cDDP back to normal levels. Consequently, overexpressing TRIM3 in drug-resistant cells facilitates PERK activation and subsequent induction of apoptosis through inhibition of GRP78, ultimately suppressing drug resistance and inducing apoptosis in CESC cells. In conclution, our study suggests that the TRIM3/GRP78 axis regulates cDDP resistance in CESC cells by modulating the downstream apoptotic pathway of ERS.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-12"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142766033","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Novel insights into RNA polymerase II transcription regulation: transcription factors, phase separation, and their roles in cardiovascular diseases. RNA 聚合酶 II 转录调控的新见解：转录因子、相分离及其在心血管疾病中的作用。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 Epub Date: 2024-11-14 DOI: 10.1139/bcb-2024-0094

Mengmeng Liu, Yingrui Li, Xin Yuan, Shunkang Rong, Jianlin Du

{"title":"Novel insights into RNA polymerase II transcription regulation: transcription factors, phase separation, and their roles in cardiovascular diseases.","authors":"Mengmeng Liu, Yingrui Li, Xin Yuan, Shunkang Rong, Jianlin Du","doi":"10.1139/bcb-2024-0094","DOIUrl":"10.1139/bcb-2024-0094","url":null,"abstract":"Transcription factors (TFs) are specialized proteins that bind DNA in a sequence-specific manner and modulate RNA polymerase II (Pol II) in multiple steps of the transcription process. Phase separation is a spontaneous or driven process that can form membrane-less organelles called condensates. By creating different liquid phases at active transcription sites, the formation of transcription condensates can reduce the water content of the condensate and lower the dielectric constant in biological systems, which in turn alters the structure and function of proteins and nucleic acids in the condensate. In RNA Pol II transcription, phase separation formation shortens the time at which TFs bind to target DNA sites and promotes transcriptional bursting. RNA Pol II transcription is engaged in developing several diseases, such as cardiovascular disease, by regulating different TFs and mediating the occurrence of phase separation. This review aims to summarize the advances in the molecular mechanisms of RNA Pol II transcriptional regulation, in particular the effect of TFs and phase separation. The role of RNA Pol II transcriptional regulation in cardiovascular disease will be elucidated, providing potential therapeutic targets for the management and treatment of cardiovascular disease.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-21"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142614125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Gallein, G protein βγ subunits inhibitor, suppresses the TGF-α-induced migration of hepatocellular carcinoma cells via inhibition of the c-Jun N-terminal kinase. G蛋白βγ亚基抑制剂Gallein通过抑制c-Jun N-末端激酶抑制TGF-α诱导的肝癌细胞迁移。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 DOI: 10.1139/bcb-2024-0141

Rie Matsushima-Nishiwaki, Yoh Honda, Haruhiko Tokuda, Osamu Kozawa

{"title":"Gallein, G protein βγ subunits inhibitor, suppresses the TGF-α-induced migration of hepatocellular carcinoma cells via inhibition of the c-Jun N-terminal kinase.","authors":"Rie Matsushima-Nishiwaki, Yoh Honda, Haruhiko Tokuda, Osamu Kozawa","doi":"10.1139/bcb-2024-0141","DOIUrl":"10.1139/bcb-2024-0141","url":null,"abstract":"G protein-coupled receptor (GPCR) signaling regulates a wide range of pathophysiological cell functions via G protein α and βγ subunits. Small molecules targeting the subunits of Gα and Gβγ have been developed as cancer therapeutics. We have previously reported that transforming growth factor-α (TGF-α) induces the migration of human hepatocellular carcinoma (HCC) HuH7 cells through the activation of AKT, p38 mitogen-activated protein kinase (MAPK), Rho-kinase, and c-Jun N-terminal kinase (JNK). This study aims to determine whether Gβγ subunits regulate the TGF-α-induced migration of HCC HuH7 cells using gallein, a Gβγ subunits inhibitor. The Janus family of tyrosine kinase/signal transducer and activator of transcription 3 (STAT3) signaling pathway was also involved in the regulation of the migration. Gallein significantly reduced the TGF-α-induced cell migration. In contrast, fluorescein, a gallein-related compound that has no effect on Gβγ subunits, failed to affect the cell migration. Gallein suppressed the TGF-α-stimulated phosphorylation of JNK without affecting the phosphorylation of epidermal growth factor receptor, AKT, p38 MAPK, target protein of Rho-kinase, and STAT3. Conversely, fluorescein did not attenuate the phosphorylation of JNK. These results strongly suggest that Gβγ subunits act as positive regulators in TGF-α-induced migration of HCC cells via the JNK signaling pathway.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-9"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142614083","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0