International Journal of Biochemistry & Cell Biology最新文献

{"title":"A modified model of PANoptosisto identify prognosis and immunotherapy response in bladder cancer","authors":"Weichao Lv ,&nbsp;Xiaohang Lei ,&nbsp;Hongyuan Wang ,&nbsp;Tongtong Wang ,&nbsp;Jianguo Zhang","doi":"10.1016/j.biocel.2024.106672","DOIUrl":"10.1016/j.biocel.2024.106672","url":null,"abstract":"<div><h3>Background</h3><div>Cell death, including apoptosis and necrosis, collectively known as widespread apoptosis. The present study aims to investigate the mechanism of action in widespread apoptosis-related modification patterns in bladder cancer.</div></div><div><h3>Methods</h3><div>Using a clinical genomics database, we obtained transcriptomic data and related clinical information of bladder cancer patients. By employing the least absolute shrinkage analysis, we were able to construct a risk model and single-cell sequencing analysis of differential genes in bladder cancer.</div></div><div><h3>Results</h3><div>Five differentially expressed genes (TMPRSS4, TPST1, FOXD1, ELOVL4, EMP1) associated with widespread apoptosis were identified as features for predicting the prognosis of bladder cancer patients. Survival curve analysis revealed significant differences in prognosis (P&lt;0.05). Additionally, multivariate Cox regression analysis determined the independent risk factor for bladder cancer prognosis as the risk score (P&lt;0.001), with high confidence in the scoring model validated internally (P&lt;0.001). Single-cell sequencing reveals high expression of CDKN2A, ERBB2, and TMPRSS4 in B cells, while HRAS is significantly expressed in fibroblasts.</div></div><div><h3>Conclusion</h3><div>PANscore, as a potential prognostic and immunotherapeutic biomarker, will provide more precise and rational basis for personalized treatment strategies</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"176 ","pages":"Article 106672"},"PeriodicalIF":3.4,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142378493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Visualizing, quantifying and mapping chromatin remodelers at work with single-molecule and single-cell imaging","authors":"Hendrik Sielaff ,&nbsp;Ziqing Winston Zhao","doi":"10.1016/j.biocel.2024.106667","DOIUrl":"10.1016/j.biocel.2024.106667","url":null,"abstract":"<div><div>Chromatin remodeling, carried out by four major subfamilies of ATP-dependent remodeler complexes across eukaryotes, alleviates the topological challenge posed by nucleosomes to regulate genome access. Recently, single-molecule and single-cell imaging techniques have been widely employed to probe this crucial process, both <em>in vitro</em> and <em>in cellulo</em>. Herein, we provide an integrated account of key recent efforts that leverage these approaches to visualize, quantify and map chromatin remodelers at work, elucidating diverse aspects of the remodeling process in both space and time, including molecular mechanisms of DNA wrapping/unwrapping, nucleosome translocation and histone exchange, dynamics of chromatin binding/target search and their intranuclear organization into hotspots or phase condensates, as well as functional coupling with transcription. The mechanistic insights and quantitative parameters revealed shed light on a multi-modal yet shared landscape for regulating remodeling across molecular and cellular scales, and pave the way for further interrogating the implications of its misregulation in disease contexts.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"176 ","pages":"Article 106667"},"PeriodicalIF":3.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142373439","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":"MIEN1 on the 17q12 amplicon facilitates the malignant behaviors of gastric cancer via activating IL-6/JAK2/STAT3 pathway","authors":"Jing Lin ,&nbsp;Dong Wang ,&nbsp;Jiahui Zhou ,&nbsp;Jing Bai ,&nbsp;Shouzhen Sun ,&nbsp;Xueyuan Jia ,&nbsp;Xiao Liang ,&nbsp;Songbin Fu ,&nbsp;Jingcui Yu","doi":"10.1016/j.biocel.2024.106666","DOIUrl":"10.1016/j.biocel.2024.106666","url":null,"abstract":"<div><div>Oncogene amplification is a significant factor contributing to poor prognosis and limited treatment in patients with advanced gastric cancer. Therefore, identifying amplified oncogenes and elucidating their oncogenic mechanisms will provide reliable therapeutic targets for the clinical treatment of gastric cancer. In this study, we identify a high amplification of 17q12, which includes five oncogenes that are co-amplified and co-overexpressed with ERBB2 using array comparative genomic hybridization, with migration and invasion enhancer 1 (MIEN1) being particularly highlighted for its clinical significance, function, and role in gastric cancer progression. By detecting MIEN1 copy number and expression level across eight gastric cancer cell lines and in tissue microarrays from 543 primary gastric cancer tissues, we found that MIEN1 amplification and overexpression correlated with sex and Lauren’s intestinal type classification of gastric cancer. Besides that, elevated MIEN1 expression was associated with poorer patient survival. In vitro experiments have shown that MIEN1 overexpression enhanced cell proliferation, invasion, and migration, whereas MIEN1 knockdown reversed these malignant phenotypes in vitro. Furthermore, MIEN1 knockdown inhibited tumorigenesis and metastasis of gastric cancer cells in nude mice. Mechanistically, MIEN1 activates the IL-6/JAK2/STAT3 signaling pathway, which drives the proliferation, invasion, and migration of gastric cancer cells. This study demonstrates that MIEN1 contributes to the malignant behavior of gastric cancer through the IL-6/JAK2/STAT3 pathway, suggesting that MIEN1 could serve as a valuable therapeutic target for gastric cancer.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"176 ","pages":"Article 106666"},"PeriodicalIF":3.4,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142331580","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":"Classical psychedelics’ action on brain monoaminergic systems","authors":"Jasmine Jade Butler ,&nbsp;Daria Ricci ,&nbsp;Chloé Aman ,&nbsp;Anna Beyeler ,&nbsp;Philippe De Deurwaerdère","doi":"10.1016/j.biocel.2024.106669","DOIUrl":"10.1016/j.biocel.2024.106669","url":null,"abstract":"<div><div>The study of the mechanism of action of classical psychedelics has gained significant interest due to their clinical potential in the treatment of several psychiatric conditions, including major depressive and anxiety disorders. These drugs bind 5-hydroxytryptamine receptors (5-HTR) including 5-HT_1AR, 5-HT_2AR, 5-HT_2BR, and/or 5-HT₂_CR, as well as other targets. 5-HTRs regulate the activity of ascending monoaminergic neurons, a mechanism primarily involved in the action of classical antidepressant drugs, antipsychotics, and drugs of abuse. Sparse neurochemical data have been produced on the control of monoaminergic neuron activity in response to classical psychedelics. Here we review the available data in order to determine whether classical psychedelics have specific neurochemical effects on serotonergic, dopaminergic, and noradrenergic neurons. The data show that these drugs have disparate effects on each monoaminergic system, demonstrating a complex response with state-dependent and region-specific effects. For instance, several psychedelics inhibit the firing of serotonergic neurons, although this is not necessarily associated with a decrease in serotonin release in all regions. Noradrenergic neuron spontaneous activity also appears to be inhibited by psychedelics, also not necessarily associated with a decrease in noradrenaline release in all regions. Psychedelics influence on dopaminergic systems is also complex as the above-mentioned 5-HTRs may have opposing effects on dopaminergic neuron activity, in a state-dependent manner. There is an apparent lack of clear neuronal signature induced by psychedelics on monoaminergic neuron activity despite specific recurrent mechanisms. This review provides a current summary of the action of psychedelics on monoamine neuromodulators serotonin, dopamine and noradrenaline, compiling reoccurring and contradictory findings demonstrating that a monoamine signature of psychedelics, if applicable, would be state- and region-dependant.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"176 ","pages":"Article 106669"},"PeriodicalIF":3.4,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142331581","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":"SUMOylation of cardiac myosin binding protein-C reduces its phosphorylation and results in impaired relaxation following treatment with isoprenaline","authors":"Alice Main,&nbsp;Sheon Mary,&nbsp;Yuan Yan Sin,&nbsp;Tom A. Wright,&nbsp;Jiayue Ling,&nbsp;Connor M. Blair,&nbsp;Godfrey L. Smith,&nbsp;Will Fuller,&nbsp;George S. Baillie","doi":"10.1016/j.biocel.2024.106668","DOIUrl":"10.1016/j.biocel.2024.106668","url":null,"abstract":"<div><div>Systolic and diastolic functions are coordinated in the heart by myofilament proteins that influence force of contraction and calcium sensitivity. Fine control of these processes is afforded by a variety of post-translation modifications that occur on specific proteins at different times during each heartbeat. Cardiac myosin binding protein-C is a sarcomeric accessory protein whose function is to interact transiently with actin, tropomyosin and myosin. Previously many different types of post-translational modification have been shown to influence the action of myosin binding protein-C and we present the first report that the protein can be modified covalently by the small ubiquitin like modifier protein tag. Analysis by mass spectrometry suggests that there are multiple modification sites on myosin binding protein-C for this tag and single point mutations did not serve to abolish the covalent addition of the small ubiquitin like modifier protein. Functionally, our data from both model human embryonic kidney cells and transfected neonatal cardiac myocytes suggests that the modification reduces phosphorylation of the filament protein on serine 282. In cardiac myocytes, the hypo-phosphorylation coincided with a significantly slower relaxation response following isoprenaline induced contraction. We hypothesise that this novel modification of myosin binding protein-C represents a new level of control that acts to alter the relaxation kinetics of cardiac myocytes.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"176 ","pages":"Article 106668"},"PeriodicalIF":3.4,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1357272524001602/pdfft?md5=ae25804bd223f4802b2c4f103ab4ecbd&pid=1-s2.0-S1357272524001602-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142315066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic perturbations associated with hIAPP-induced insulin resistance in skeletal muscles: Implications to the development of type 2 diabetes","authors":"Arya R. Naik ,&nbsp;Shreyada N. Save ,&nbsp;Soumya S. Sahoo ,&nbsp;Saurabh S. Yadav ,&nbsp;Ashutosh Kumar ,&nbsp;Jeetender Chugh ,&nbsp;Shilpy Sharma","doi":"10.1016/j.biocel.2024.106665","DOIUrl":"10.1016/j.biocel.2024.106665","url":null,"abstract":"<div><div>The human islet amyloid polypeptide (hIAPP) tends to misfold and self-assemble to form amyloid fibrils, which has been associated with the loss of function and viability of pancreatic β-cells in type 2 diabetes mellitus (T2DM). The role of hIAPP in the development of insulin resistance (a hallmark of T2DM) in skeletal muscles – the major sites for glucose utilization – needs further investigation. Even though, insulin-resistant conditions have been known to stimulate hIAPP aggregation, the events that lead to the development of insulin resistance due to hIAPP aggregation in skeletal muscles remain unidentified. Here, we have attempted to identify metabolic perturbations in L6 myotubes that were exposed to increasing concentrations of recombinant hIAPP for different time durations. It was observed that hIAPP exposure was associated with increased mitochondrial and cellular ROS levels, loss in mitochondrial membrane potential and viability of the myotubes. Metabolomic investigations of hIAPP-treated myotubes revealed significant perturbations in o-phosphocholine, sn-glycero-3-phosphocholine and dimethylamine levels (p &lt; 0.05). Therefore, we anticipate that defects in glycerophospholipid metabolism and the associated oxidative stress and membrane damage may play key roles in the development of insulin resistance due to protein misfolding in skeletal muscles. In summary, the perturbed metabolites and their pathways have not only the potential to be used as early biomarkers to predict the onset of insulin resistance and T2DM but also as therapeutic targets for the effective management of the same.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"176 ","pages":"Article 106665"},"PeriodicalIF":3.4,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142331582","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":"Revisiting serotonin’s role in spatial memory: A call for sensitive analytical approaches","authors":"Paulina Kazmierska-Grebowska ,&nbsp;Witold Żakowski ,&nbsp;Dorota Myślińska ,&nbsp;Ravindra Sahu ,&nbsp;Maciej M. Jankowski","doi":"10.1016/j.biocel.2024.106663","DOIUrl":"10.1016/j.biocel.2024.106663","url":null,"abstract":"<div><div>The serotonergic system is involved in various psychiatric and neurological conditions, with serotonergic drugs often used in treatment. These conditions frequently affect spatial memory, which can serve as a model of declarative memory due to well-known cellular components and advanced methods that track neural activity and behavior with high temporal resolution. However, most findings on serotonin's effects on spatial learning and memory come from studies lacking refined analytical techniques and modern approaches needed to uncover the underlying neuronal mechanisms. This In Focus review critically investigates available studies to identify areas for further exploration. It finds that well-established behavioral models could yield more insights with modern tracking and data analysis approaches, while the cellular aspects of spatial memory remain underexplored. The review highlights the complex role of serotonin in spatial memory, which holds the potential for better understanding and treating memory-related disorders.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"176 ","pages":"Article 106663"},"PeriodicalIF":3.4,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142315079","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":"High glucose induces DNA methyltransferase 1 dependent epigenetic reprogramming of the endothelial exosome proteome in type 2 diabetes","authors":"Sampara Vasishta ,&nbsp;Shruthi Ammankallu ,&nbsp;Ganesha Poojary ,&nbsp;Sarah Michael Gomes ,&nbsp;Kailash Ganesh ,&nbsp;Shashikiran Umakanth ,&nbsp;Prashanth Adiga ,&nbsp;Dinesh Upadhya ,&nbsp;Thottethodi Subrahmanya Keshava Prasad ,&nbsp;Manjunath B. Joshi","doi":"10.1016/j.biocel.2024.106664","DOIUrl":"10.1016/j.biocel.2024.106664","url":null,"abstract":"<div><div>In response to hyperglycemia, endothelial cells (ECs) release exosomes with altered protein content and contribute to paracrine signalling, subsequently leading to vascular dysfunction in type 2 diabetes (T2D). High glucose reprograms DNA methylation patterns in various cell/tissue types, including ECs, resulting in pathologically relevant changes in cellular and extracellular proteome. However, DNA methylation-based proteome reprogramming in endothelial exosomes and associated pathological implications in T2D are not known. Hence, in the present study, we used Human umbilical vein endothelial cells (HUVECs), High Fat Diet (HFD) induced diabetic mice (C57BL/6) and clinical models to understand epigenetic basis of exosome proteome regulation in T2D pathogenesis . Exosomes were isolated by size exclusion chromatography and subjected to tandem mass tag (TMT) labelled quantitative proteomics and bioinformatics analysis. Immunoblotting was performed to validate exosome protein signature in clinically characterized individuals with T2D. We observed ECs cultured in high glucose and aortic ECs from HFD mouse expressed elevated DNA methyltransferase1 (DNMT1) levels. Quantitative proteomics of exosomes isolated from ECs treated with high glucose and overexpressing DNMT1 showed significant alterations in both protein levels and post translational modifications which were aligned to T2D associated vascular functions. Based on ontology and gene-function-disease interaction analysis, differentially expressed exosome proteins such as Thrombospondin1, Pentraxin3 and Cystatin C related to vascular complications were significantly increased in HUVECs treated with high glucose and HFD animals and T2D individuals with higher levels of glycated hemoglobin. These proteins were reduced upon treatment with 5-Aza-2’-deoxycytidine. Our study shows epigenetic regulation of exosome proteome in T2D associated vascular complications.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"176 ","pages":"Article 106664"},"PeriodicalIF":3.4,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1357272524001560/pdfft?md5=09356ee9f592b8107927607f95021599&pid=1-s2.0-S1357272524001560-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142299984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PIAS1 S510G variant acts as a genetic modifier of spinocerebellar ataxia type 3 by selectively impairing mutant ataxin-3 proteostasis","authors":"Yi-Ching Chang ,&nbsp;Yao-Chou Tsai ,&nbsp;En-Cheng Chang ,&nbsp;Yu-Chien Hsu ,&nbsp;Yi-Ru Huang ,&nbsp;Yan-Hua Lee ,&nbsp;Yu-Shuen Tsai ,&nbsp;Yin-Quan Chen ,&nbsp;Yi-Chung Lee ,&nbsp;Yi-Chu Liao ,&nbsp;Jean-Cheng Kuo ,&nbsp;Ming-Tsan Su ,&nbsp;Ueng-Cheng Yang ,&nbsp;Yijuang Chern ,&nbsp;Tzu-Hao Cheng","doi":"10.1016/j.biocel.2024.106662","DOIUrl":"10.1016/j.biocel.2024.106662","url":null,"abstract":"<div><div>Dysregulated protein homeostasis, characterized by abnormal protein accumulation and aggregation, is a key contributor to the progression of neurodegenerative disorders such as Huntington's disease and spinocerebellar ataxia type 3 (SCA3). Previous studies have identified <em>PIAS1</em> gene variants in patients with late-onset SCA3 and Huntington's disease. This study aims to elucidate the role of <em>PIAS1</em> and its S510G variant in modulating the pathogenic mechanisms of SCA3. Through <em>in vitro</em> biochemical analyses and <em>in vivo</em> assays, we demonstrate that PIAS1 stabilizes both wild-type and mutant ataxin-3 (ATXN3). The <em>PIAS1</em> S510G variant, however, selectively reduces the stability and SUMOylation of mutant ATXN3, thereby decreasing its aggregation and toxicity while maintaining the stability of wild-type ATXN3. This effect is mediated by a weakened interaction with the SUMO-conjugating enzyme UBC9 in the presence of mutant ATXN3. In Drosophila models, downregulation of dPIAS1 resulted in reduced levels of mutant ATXN3 and alleviated associated phenotypes, including retinal degeneration and motor dysfunction. Our findings suggest that the <em>PIAS1</em> S510G variant acts as a genetic modifier of SCA3, highlighting the potential of targeting SUMOylation as a therapeutic strategy for this disease.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"176 ","pages":"Article 106662"},"PeriodicalIF":3.4,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1357272524001547/pdfft?md5=ee2968809e055b854132c73ad3383723&pid=1-s2.0-S1357272524001547-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142262019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unveiling the role of taurine and SLC6A6 in tumor immune evasion: Implications for gastric cancer therapy","authors":"Jianqiao Shentu,&nbsp;Xinming Su,&nbsp;Yueqi Yu,&nbsp;Shiwei Duan","doi":"10.1016/j.biocel.2024.106661","DOIUrl":"10.1016/j.biocel.2024.106661","url":null,"abstract":"<div><p>Metabolic changes are key drivers of tumor progression. Understanding how metabolic reprogramming promotes tumor development and identifying key metabolic activities are essential for improving tumor diagnosis and treatment. Among the numerous transporters in the body, solute carriers (SLCs) are particularly significant, often overexpressed in cancer cells to meet the tumor's demand for nutrients and energy. While the role of SLCs in nutrient absorption within the gastrointestinal tract is well-established, their specific role in gastric cancer (GC) remains unclear. Recently, Xiaodi Zhao's team investigated the critical role of taurine and its transporter, SLC6A6, in anti-tumor immunity and clinical outcomes. Notably, this research marks the first instance of taurine exhibiting a dual role. It promotes tumor growth in immunodeficient mice while inhibiting it in immunocompetent mice. The study found that taurine exerts its anti-cancer effects by modulating CD8⁺ T cells rather than directly inhibiting tumor cells, revealing the SP1-SLC6A6 axis as a key mechanism behind chemotherapy-induced immune evasion. Our work further explored the potential, advantages, and challenges of using taurine and SLC6A6 as biomarkers and therapeutic targets in gastric cancer. We aim to underscore their importance in both basic research and clinical applications, providing valuable insights and guidance for future investigations.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"176 ","pages":"Article 106661"},"PeriodicalIF":3.4,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142172564","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}