International Journal of Biochemistry & Cell Biology最新文献

{"title":"TFAP2C/FLT3 axis reduces ferroptosis in breast cancer cells by inhibiting mitochondrial autophagy","authors":"Jiayue Shen ,&nbsp;Yali He ,&nbsp;Bingchuan Zhou ,&nbsp;Huabo Qin ,&nbsp;Shuai Zhang ,&nbsp;Zixiang Huang ,&nbsp;Xiangcheng Zhang","doi":"10.1016/j.biocel.2024.106691","DOIUrl":"10.1016/j.biocel.2024.106691","url":null,"abstract":"<div><h3>Background</h3><div>FMS-like tyrosine kinase 3 (FLT3), a key target protein for treating acute myeloid leukemia, has recently been found to be closely related to ferroptosis in breast cancer (BC). However, the mechanism by which FLT3 regulates ferroptosis in BC remains unknown. Whether this regulatory relationship can be exploited for BC treatment needs further exploration.</div></div><div><h3>Methods</h3><div>This study combined analysis from The Cancer Genome Atlas database with immunohistochemistry/quantitative reverse transcription-PCR/Western blot experiments to verify the expression of FLT3 in BC. FLT3 knockdown/overexpression plasmids were used in conjunction with mitochondrial autophagy inducers to treat BC cells, analyzing the effects of FLT3 on autophagy and ferroptosis. Key transcription factors for FLT3 were determined through predictions from the KnockTF database and dual luciferase/chromatin immunoprecipitation experiments, further analyzing the impact of this regulatory axis on autophagy and ferroptosis in BC cells.</div></div><div><h3>Results</h3><div>FLT3 was significantly overexpressed in BC tissues and cells. Overexpression of FLT3 could inhibit autophagy and ferroptosis in BC cells, a regulation that was restored upon the addition of mitochondrial autophagy inducers. Additionally, transcription factor AP-2 gamma (TFAP2C) could mediate the transcriptional activation of FLT3, further inhibiting ferroptosis induced by mitochondrial autophagy.</div></div><div><h3>Conclusion</h3><div>The TFAP2C/FLT3 axis reduced ferroptosis in BC cells by inhibiting mitochondrial autophagy. These research findings elucidated the mechanism by which FLT3 regulated ferroptosis in BC and provided potential targets for BC treatment.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"177 ","pages":"Article 106691"},"PeriodicalIF":3.4,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142631041","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}

{"title":"Long non-coding RNA AC105118.1 affects glycolysis to facilitate oxaliplatin resistance in colorectal cancer cells by modulating the miR-378a-3p/KIF26B axis","authors":"Yong Zhang,&nbsp;Zhiling Shen,&nbsp;Xiaodong Han,&nbsp;Yachao Wu,&nbsp;Tianchen Huang","doi":"10.1016/j.biocel.2024.106692","DOIUrl":"10.1016/j.biocel.2024.106692","url":null,"abstract":"<div><h3>Background</h3><div>Oxaliplatin is a first-line chemotherapy drug for colorectal cancer (CRC), but many patients eventually lose treatment efficacy due to acquired resistance. AC105118.1 is a long non-coding RNA with unknown biological function. This research attempts to probe into the molecular regulatory mechanism of AC105118.1 in CRC oxaliplatin resistance.</div></div><div><h3>Methods</h3><div>The expression level of AC105118.1 in CRC tissues and cells was measured based on The Cancer Genome Atlas (TCGA) data and quantitative reverse transcription polymerase chain reaction (qRT-PCR). We utilized dual-luciferase assay and RNA immunoprecipitation to analyze the interaction between AC105118.1, miR-378a-3p, and their downstream target KIF26B. CCK-8, colony formation assay, and flow cytometry were employed to assess the half inhibitory concentration (IC₅₀), cell proliferation, and apoptosis rate of HCT116/L-OHP cells treated with oxaliplatin. The glycolysis evaluation was completed by measuring the extracellular acidification rate (ECAR), glucose consumption, lactate production, and glycolysis-related proteins (HK2, GLUT1, and LDHA). TUNEL staining was used to detect the level of apoptosis.</div></div><div><h3>Results</h3><div>AC105118.1 was specifically upregulated in CRC tissues and cells. AC105118.1 indirectly facilitated the expression of miRNA target gene KIF26B by sequestering miR-378a-3p. In HCT116/L-OHP cells, transfection with si-AC105118.1 resulted in a decrease in glycolysis level, a lower maximum IC₅₀ required for oxaliplatin-treated cells, inhibited cell proliferation, and an increase in apoptosis rate. All of these effects were alleviated when simultaneously transfecting miR-378a-3p inhibitor or oe-KIF26B. Knockdown of AC105118.1 significantly inhibited oxaliplatin resistance to CRC in mice.</div></div><div><h3>Conclusion</h3><div>AC105118.1 facilitates glycolysis and increases CRC cells’ resistance to oxaliplatin by targeting the miR-378a-3p/KIF26B axis. The present work shed new insights into the function and mechanism of AC105118.1 in molecular function and suggested that the AC105118.1/miR-378a-3p/KIF26B axis is a promising target for intervening CRC oxaliplatin resistance.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"177 ","pages":"Article 106692"},"PeriodicalIF":3.4,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142630904","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}

{"title":"Myc functions downstream of InR and their concurrent upregulation additively restricts pathogenesis of human poly(Q) disorders in Drosophila disease models","authors":"Shweta Tandon ,&nbsp;Surajit Sarkar","doi":"10.1016/j.biocel.2024.106690","DOIUrl":"10.1016/j.biocel.2024.106690","url":null,"abstract":"<div><div>Human polyglutamine [poly(Q)] disorders are caused by abnormal expansion of CAG repeats in one gene (disease specific), yet a plethora of cellular pathways are found to be involved in their pathogenesis and progression. Despite the tremendous effort, all pursuits for the development of intervention therapy against these disorders seem futile. Recent reports suggest combination therapy as a potential strategy to combat the complex pathogenesis of such neurodegenerative disorders. The present study attempted to identify a combinatorial intervention strategy against human poly(Q) disorders in <em>Drosophila</em> disease models. Due to its immense potential to be stimulated by drugs, the evolutionarily conserved insulin signalling cascade which is well-established modifier of human poly(Q) pathogenesis was selected for the study. Genetic screening studies identified <em>Drosophila</em> Myc as a potential partner of insulin receptor (InR) that conferred additive rescue against poly(Q) induced neurodegeneration. Comprehensive analyses demonstrated InR and Myc to confer additive rescue against several events of pathogenesis, including aggregation of expanded poly(Q) containing proteins, transcriptional dysregulation, upsurge of cell death cascades, etc. Also, the synergistic rescue efficiency of InR and Myc was equally efficient in mitigating poly(Q) induced structural and functional deficits. The study also demonstrates that Myc functions downstream of InR signalling cascade to deliver rescue against human poly(Q) mediated toxicity in <em>Drosophila</em> disease models. In conclusion, the present study suggests that InR and Myc have the potential to be developed as a combinatorial therapeutic approach against human poly(Q) diseases.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"177 ","pages":"Article 106690"},"PeriodicalIF":3.4,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142630995","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}

{"title":"Integrative multi-omics and big data analysis of global nutrition and radiotherapy trends","authors":"Sibo Meng ,&nbsp;Dizhi Jiang ,&nbsp;Guanghui Yang ,&nbsp;Kaiyue Guo ,&nbsp;Enhao Yu ,&nbsp;Yun Wang ,&nbsp;Linli Qu ,&nbsp;Jiaxin Li","doi":"10.1016/j.biocel.2024.106687","DOIUrl":"10.1016/j.biocel.2024.106687","url":null,"abstract":"<div><h3>Background</h3><div>Radiotherapy serves as a crucial modality in cancer treatment, frequently synergizing with other therapies to enhance patient outcomes. Unfortunately, radiotherapy is often accompanied by nutritional impairments, including dysphagia and malnutrition, which hinder patient recovery and treatment efficacy. Moreover, nutritional abnormalities accompanied by metabolic reprogramming may lead to alterations across multiple omics domains. Consequently, big data analysis on radiotherapy and nutrition is imperative.</div></div><div><h3>Objective</h3><div>This study employs bibliometric analysis to visually showcase the current research landscape and trending hotspots in the intersection of nutrition and radiotherapy.</div></div><div><h3>Methods</h3><div>Leveraging the Web of Science Core Collection, we screened and analyzed 4379 publications related to nutrition and radiotherapy published between 2004 and 2023. Utilizing VOSviewer, Bibliometrix, and Citespace software, we conducted bibliometric analysis and visualization of countries, institutions, authors, and keywords.</div></div><div><h3>Results</h3><div>Our analysis reveals a substantial increase in publications concerning nutrition and radiotherapy, with the United States and China leading in both publication volume and citation impact. The research focus has gradually shifted from phenomenological studies to mechanistic investigations, as evidenced by changes in keyword usage. While confirming the influence of nutritional status on radiotherapy outcomes, we also identified potential links to genomics, proteomics, metabolomics, and other omics disciplines.</div></div><div><h3>Conclusion</h3><div>This study emphasizes the growing attention to the interplay between nutrition and radiotherapy in cancer treatment. Our findings suggest that further integration of multi-omics analysis can enhance understanding of the mechanisms underlying these interactions, providing a foundation for advancing cancer diagnosis and treatment strategies in the future.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"177 ","pages":"Article 106687"},"PeriodicalIF":3.4,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142631222","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}

{"title":"Mitochondrial E3 ligase TRIM71 affects mitochondrial complex assembly and sensitizes dopaminergic neuronal cells to apoptosis in Parkinson’s Disease (PD)","authors":"Shanikumar Goyani,&nbsp;Shatakshi Shukla,&nbsp;Minal Mane,&nbsp;M.V. Saranga,&nbsp;Nisha Chandak,&nbsp;Anjali Shinde,&nbsp;Fatema Currim,&nbsp;Jyoti Singh,&nbsp;Rajesh Singh","doi":"10.1016/j.biocel.2024.106689","DOIUrl":"10.1016/j.biocel.2024.106689","url":null,"abstract":"<div><div>Parkinson’s Disease (PD) is a chronic neurodegenerative disorder that impacts the substantia niagra region of the midbrain leading to impaired motor as well as non-motor symptoms of the central nervous system (CNS). Mitochondrial dysfunction has been characterized as the primary cause of dopaminergic neuronal loss, however, the molecular mechanisms leading to mitochondrial dysfunction are not completely understood. PARKIN, E3 ubiquitin ligase, plays a crucial role in maintaining mitochondrial quality control, albeit the role of other E3 ligases in regulating mitochondrial functions is not understood. In the current study, we explored the implication of TRIM71, E3 ubiquitin ligase, in the modulation of mitochondrial functions and neuronal death in PD stress conditions induced by rotenone and 6-OHDA. Ectopic expression of TRIM71 in SH-SY5Y dopaminergic neuronal cells sensitizes to PD stress-induced cell death, while its knock-down rescues neuronal cell death. TRIM71 turnover is enhanced in neurons under PD stress conditions. TRIM71 predominantly localizes on the outer mitochondrial membrane and translocation increases during PD stress conditions. TRIM71 regulates mitochondrial complex I and IV assembly and activity. TRIM71 knock-down decreases mitochondrial ROS and enhances ATP level as well as mitochondrial membrane potential in PD stress conditions. TRIM71-mediated mitochondrial ROS and cell death were rescued by mitoTEMPO, a mitochondrial-targeted antioxidant. Altogether, the evidence strongly suggests TRIM71-mediated modulation of mitochondrial functions and neuronal apoptosis in PD stress conditions.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"177 ","pages":"Article 106689"},"PeriodicalIF":3.4,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142630907","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}

{"title":"Integrated stress response-upregulated mitochondrial SLC1A5var enhances glucose dependency in human breast cancer cells in vitro","authors":"Sheng-Fan Wang ,&nbsp;Yu-Chieh Ho ,&nbsp;Chian-Ying Chou ,&nbsp;Yuh-Lih Chang ,&nbsp;Hsin-Chen Lee ,&nbsp;Ling-Ming Tseng","doi":"10.1016/j.biocel.2024.106688","DOIUrl":"10.1016/j.biocel.2024.106688","url":null,"abstract":"<div><div>Breast cancer is the most commonly diagnosed cancer among women. The growth of triple-negative breast cancer (TNBC) cells is glucose-dependent. The integrated stress response (ISR) is a cellular stress response to glucose depletion. The ISR-solute carrier family 7 member 11 pathway is activated during glucose depletion and contributes to glucose dependence by decreasing intracellular glutamate levels. Solute carrier family 1 member 5 (SLC1A5) and the mitochondrial solute carrier family 1 member 5 variant (SLC1A5var) are glutamine transporters that play essential roles in the reprogramming of cancer metabolism. However, whether ISR can regulate mitochondrial SLC1A5var expression and further affect glucose dependence remains unclear. Glucose depletion-, oligomycin-, and salubrinal-activated activating transcription factor-4 (ATF4) induced SLC1A5var expression. ATF4 is critical for SLC1A5var regulation, as it binds to specific regulatory elements in its promoter. SLC1A5var knockdown decreases glucose depletion-induced cell death, whereas SLC1A5var overexpression increases glucose depletion-induced cell death in TNBC cells. SLC1A5var knockdown reduced cancer cell proliferation, colony formation, and migration, whereas SLC1A5var overexpression increased cell proliferation and migration. Moreover, the knockdown of SLC1A5var reduces the oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) while increasing the maximal OCR and ECAR under glucose depletion. These results suggest that activated ISR-induced increased expression of SLC1A5var may regulate mitochondrial oxidative phosphorylation and glycolytic metabolic characteristics to enhance glucose depletion-induced cell death. In conclusion, SLC1A5var plays a vital role in metabolic reprogramming and may be a potential target for breast cancer treatment.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"177 ","pages":"Article 106688"},"PeriodicalIF":3.4,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142591925","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}

{"title":"Corrigendum to “Dual blockade of the A1 and A2A adenosine receptor prevents amyloid beta toxicity in neuroblastoma cells exposed to aluminum chloride” [Int. J. Biochem. Cell Biol. 54 (2014) 122–136]","authors":"Salvatore Giunta ,&nbsp;Violetta Andriolo ,&nbsp;Alessandro Castorina","doi":"10.1016/j.biocel.2024.106677","DOIUrl":"10.1016/j.biocel.2024.106677","url":null,"abstract":"","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"176 ","pages":"Article 106677"},"PeriodicalIF":3.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142479639","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}

{"title":"Corrigendum to “15-lipoxygenase-1/15-hydroxyeicosatetraenoic acid promotes hepatocellular cancer cells growth through protein kinase B and heat shock protein 90 complex activation” [Int. J. Biochem. Cell Biol. 45 (2013) 1031–41]","authors":"Jun Ma ,&nbsp;Lei Zhang ,&nbsp;Jianguo Zhang ,&nbsp;Mengmeng Liu ,&nbsp;Liuping Wei ,&nbsp;Tingting Shen ,&nbsp;Cui Ma ,&nbsp;Yanyan Wang ,&nbsp;Yingli Chen ,&nbsp;Daling Zhu","doi":"10.1016/j.biocel.2024.106670","DOIUrl":"10.1016/j.biocel.2024.106670","url":null,"abstract":"","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"176 ","pages":"Article 106670"},"PeriodicalIF":3.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142378494","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}

{"title":"Retraction notice to “Downregulation of Rab23 inhibits proliferation, invasion, and metastasis of human ovarian cancer” [Int. J. Biochem. Cell Biol. 116 (2019) 105617]","authors":"Lingling Gao ,&nbsp;Mingjun Zheng ,&nbsp;Qian Guo ,&nbsp;Xin Nie ,&nbsp;Xiao Li ,&nbsp;Yingying Hao ,&nbsp;Juanjuan Liu ,&nbsp;Liancheng Zhu ,&nbsp;Bei Lin","doi":"10.1016/j.biocel.2024.106673","DOIUrl":"10.1016/j.biocel.2024.106673","url":null,"abstract":"","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"176 ","pages":"Article 106673"},"PeriodicalIF":3.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142394891","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}

{"title":"Retraction notice to “Nucleocapsid protein of SARS-CoV activates the expression of cyclooxygenase-2 by binding directly to regulatory elements for nuclear factor-kappa B and CCAAT/enhancer binding protein” [Int. J. Biochem. Cell Biol. 38 (2006) 1417–1428]","authors":"Xiaohong Yan,&nbsp;Qian Hao,&nbsp;Yongxin Mu,&nbsp;Khalid Amine Timani,&nbsp;Linbai Ye,&nbsp;Ying Zhu,&nbsp;Jianguo Wu","doi":"10.1016/j.biocel.2024.106674","DOIUrl":"10.1016/j.biocel.2024.106674","url":null,"abstract":"","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"176 ","pages":"Article 106674"},"PeriodicalIF":3.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142512229","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}