Biochemistry and Cell Biology最新文献_第2页

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

Establishment of immortalized porcine intramuscular preadipocytes for the study of lipid metabolism. 永生化猪肌内前体脂肪细胞的建立及脂质代谢研究。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 DOI: 10.1139/bcb-2024-0174

Briana Locke, Ray Lu

引用次数: 0

Retraction: MicroRNA-24 alleviates isoflurane-induced neurotoxicity in rat hippocampus via attenuation of oxidative stress. 撤回：MicroRNA-24通过减轻氧化应激减轻异氟醚诱导的大鼠海马神经毒性

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 DOI: 10.1139/bcb-2025-0018

引用次数: 0

Doxorubicin, a DNA intercalator, inhibits transcription elongation. 阿霉素是一种DNA插入剂，可抑制转录延伸。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 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

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

Retraction: PYGB facilitates cell proliferation and invasiveness in non-small cell lung cancer by activating the Wnt-β-catenin signaling pathway. 撤回：PYGB通过激活Wnt-β-catenin信号通路促进非小细胞肺癌细胞增殖和侵袭性。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 DOI: 10.1139/bcb-2025-0022

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

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

O-GlcNAcylation of epidermal growth factor receptor and glucose transporter 1 prevents their intrinsic down regulation in breast cancer cells. 在乳腺癌细胞中，表皮生长因子受体和葡萄糖转运蛋白1的o - glcn酰化阻止了它们的内在下调。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 DOI: 10.1139/bcb-2025-0055

G Pauline Padilla-Meier, Yeshika Bhatia, Suresh Mishra

{"title":"O-GlcNAcylation of epidermal growth factor receptor and glucose transporter 1 prevents their intrinsic down regulation in breast cancer cells.","authors":"G Pauline Padilla-Meier, Yeshika Bhatia, Suresh Mishra","doi":"10.1139/bcb-2025-0055","DOIUrl":"10.1139/bcb-2025-0055","url":null,"abstract":"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.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-13"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144075765","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

Retraction: Active vitamin D activates chondrocyte autophagy to reduce osteoarthritis via mediating the AMPK-mTOR signaling pathway. 撤回：活性维生素D通过介导AMPK-mTOR信号通路激活软骨细胞自噬，减少骨关节炎。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 DOI: 10.1139/bcb-2025-0020

引用次数: 0