Cellular & Molecular Biology Letters最新文献

{"title":"Research progress of MUC1 in genitourinary cancers.","authors":"Weipu Mao, Houliang Zhang, Keyi Wang, Jiang Geng, Jianping Wu","doi":"10.1186/s11658-024-00654-x","DOIUrl":"10.1186/s11658-024-00654-x","url":null,"abstract":"<p><p>MUC1 is a highly glycosylated transmembrane protein with a high molecular weight. It plays a role in lubricating and protecting mucosal epithelium, participates in epithelial cell renewal and differentiation, and regulates cell adhesion, signal transduction, and immune response. MUC1 is expressed in both normal and malignant epithelial cells, and plays an important role in the diagnosis, prognosis prediction and clinical monitoring of a variety of tumors and is expected to be a new therapeutic target. This article reviews the structural features, expression regulation mechanism, and research progress of MUC1 in the development of genitourinary cancers and its clinical applications.</p>","PeriodicalId":9688,"journal":{"name":"Cellular & Molecular Biology Letters","volume":null,"pages":null},"PeriodicalIF":9.2,"publicationDate":"2024-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11533421/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142567411","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chemokine CXCL13-CXCR5 signaling in neuroinflammation and pathogenesis of chronic pain and neurological diseases.","authors":"Kaige Zheng, Muyan Chen, Xingjianyuan Xu, Peiyi Li, Chengyu Yin, Jie Wang, Boyi Liu","doi":"10.1186/s11658-024-00653-y","DOIUrl":"10.1186/s11658-024-00653-y","url":null,"abstract":"<p><p>Chronic pain dramatically affects life qualities of the sufferers. It has posed a heavy burden to both patients and the health care system. However, the current treatments for chronic pain are usually insufficient and cause many unwanted side effects. Chemokine C-X-C motif ligand 13 (CXCL13), formerly recognized as a B cell chemokine, binds with the cognate receptor CXCR5, a G-protein-coupled receptor (GPCR), to participate in immune cell recruitments and immune modulations. Recent studies further demonstrated that CXCL13-CXCR5 signaling is implicated in chronic pain via promoting neuroimmune interaction and neuroinflammation in the sensory system. In addition, some latest work also pointed out the involvement of CXCL13-CXCR5 in the pathogenesis of certain neurological diseases, including ischemic stroke and amyotrophic lateral sclerosis. Therefore, we aim to outline the recent findings in regard to the involvement of CXCL13-CXCR5 signaling in chronic pain as well as certain neurological diseases, with the focus on how this chemokine signaling contributes to the pathogenesis of these neurological diseases via regulating neuroimmune interaction and neuroinflammation. Strategies that can specifically target CXCL13-CXCR5 signaling in distinct locations may provide new therapeutic options for these neurological diseases.</p>","PeriodicalId":9688,"journal":{"name":"Cellular & Molecular Biology Letters","volume":null,"pages":null},"PeriodicalIF":9.2,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11523778/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142544022","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transactivation of the EGF receptor as a novel desensitization mechanism for G protein-coupled receptors, illustrated by dopamine D2-like and β₂ adrenergic receptors.","authors":"Dooti Kundu, Xiao Min, Shujie Wang, Lulu Peng, Xinru Tian, Mengling Wang, Kyeong-Man Kim","doi":"10.1186/s11658-024-00652-z","DOIUrl":"10.1186/s11658-024-00652-z","url":null,"abstract":"<p><p>Transactivation of epidermal growth factor receptors (EGFR) provides intricate control over multiple regulatory cellular processes that merge the diversity of G protein-coupled receptors (GPCRs) with the robust signaling capacities of receptor tyrosine kinases. Contrary to the typical assertions, our findings demonstrate that EGFR transactivation contributes to the desensitization of GPCRs. Repeated agonist stimulation of certain GPCRs enhanced EGFR transactivation, triggering a series of cellular events associated with GPCR desensitization. This effect was observed in receptors undergoing desensitization (D₃R, K149C-D₂R, β₂AR) but not in those resistant to desensitization (D₂R, C147K-D₃R, D₄R, β₂AR mutants lacking GRK2 or GRK6 phosphorylation sites). The EGFR inhibitor AG1478 prevented both desensitization and the associated cellular events. Similarly, these cellular events were also observed when cells were treated with EGF, but only in GPCRs that undergo desensitization. These findings suggest that EGFR transactivation diversifies pathways involved in ERK activation through the EGFR signaling system and also mediates GPCR desensitization. Alongside the widely accepted steric hindrance model, these findings offer new insights into understanding the mechanisms of GPCR desensitization, which occurs through complex cellular processes.</p>","PeriodicalId":9688,"journal":{"name":"Cellular & Molecular Biology Letters","volume":null,"pages":null},"PeriodicalIF":9.2,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11514929/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142521129","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Extracellular vesicles derived from CD4 ⁺ T cells carry DGKK to promote sepsis-induced lung injury by regulating oxidative stress and inflammation.","authors":"Guo-Wei Tu, Yi Zhang, Jie-Fei Ma, Jun-Yi Hou, Guang-Wei Hao, Ying Su, Jing-Chao Luo, Lulu Sheng, Luo Z","doi":"10.1186/s11658-024-00648-9","DOIUrl":"10.1186/s11658-024-00648-9","url":null,"abstract":"","PeriodicalId":9688,"journal":{"name":"Cellular & Molecular Biology Letters","volume":null,"pages":null},"PeriodicalIF":9.2,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11520461/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142521128","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Research progress of ankyrin repeat domain 1 protein: an updated review.","authors":"Xusan Xu, Xiaoxia Wang, Yu Li, Riling Chen, Houlang Wen, Yajun Wang, Guoda Ma","doi":"10.1186/s11658-024-00647-w","DOIUrl":"https://doi.org/10.1186/s11658-024-00647-w","url":null,"abstract":"<p><p>Ankyrin repeat domain 1 (Ankrd1) is an acute response protein that belongs to the muscle ankyrin repeat protein (MARP) family. Accumulating evidence has revealed that Ankrd1 plays a crucial role in a wide range of biological processes and diseases. This review consolidates current knowledge on Ankrd1's functions in myocardium and skeletal muscle development, neurogenesis, cancer, bone formation, angiogenesis, wound healing, fibrosis, apoptosis, inflammation, and infection. The comprehensive profile of Ankrd1 in cardiovascular diseases, myopathy, and its potential as a candidate prognostic and diagnostic biomarker are also discussed. In the future, more studies of Ankrd1 are warranted to clarify its role in diseases and assess its potential as a therapeutic target.</p>","PeriodicalId":9688,"journal":{"name":"Cellular & Molecular Biology Letters","volume":null,"pages":null},"PeriodicalIF":9.2,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11488291/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142459009","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Caspase-8 in inflammatory diseases: a potential therapeutic target.","authors":"Wangzheqi Zhang, Chenglong Zhu, Yan Liao, Miao Zhou, Wenyun Xu, Zui Zou","doi":"10.1186/s11658-024-00646-x","DOIUrl":"10.1186/s11658-024-00646-x","url":null,"abstract":"<p><p>Caspase-8, a renowned cysteine-aspartic protease within its enzyme family, initially garnered attention for its regulatory role in extrinsic apoptosis. With advancing research, a growing body of evidence has substantiated its involvement in other cell death processes, such as pyroptosis and necroptosis, as well as its modulatory effects on inflammasomes and proinflammatory cytokines. PANoptosis, an emerging concept of cell death, encompasses pyroptosis, apoptosis, and necroptosis, providing insight into the often overlapping cellular mortality observed during disease progression. The activation or deficiency of caspase-8 enzymatic activity is closely linked to PANoptosis, positioning caspase-8 as a key regulator of cell survival or death across various physiological and pathological processes. Aberrant expression of caspase-8 is closely associated with the development and progression of a range of inflammatory diseases, including immune system disorders, neurodegenerative diseases (NDDs), sepsis, and cancer. This paper delves into the regulatory role and impact of caspase-8 in these conditions, aiming to elucidate potential therapeutic strategies for the future intervention.</p>","PeriodicalId":9688,"journal":{"name":"Cellular & Molecular Biology Letters","volume":null,"pages":null},"PeriodicalIF":9.2,"publicationDate":"2024-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11463096/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142388336","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endometrial regeneration cell-derived exosomes loaded with siSLAMF6 inhibit cardiac allograft rejection through the suppression of desialylation modification.","authors":"Yini Xu, Shaohua Ren, Hongda Wang, Yafei Qin, Tong Liu, Chenglu Sun, Yiyi Xiao, Bo Shao, Jingyi Zhang, Qiang Chen, Pengyu Zhao, Guangmei Yang, Xu Liu, Hao Wang","doi":"10.1186/s11658-024-00645-y","DOIUrl":"10.1186/s11658-024-00645-y","url":null,"abstract":"<p><strong>Backgrounds: </strong>Acute transplant rejection is a major component of poor prognoses for organ transplantation. Owing to the multiple complex mechanisms involved, new treatments are still under exploration. Endometrial regenerative cells (ERCs) have been widely used in various refractory immune-related diseases, but the role of ERC-derived exosomes (ERC-Exos) in alleviating transplant rejection has not been extensively studied. Signaling lymphocyte activation molecule family 6 (SLAMF6) plays an important role in regulating immune responses. In this study, we explored the main mechanism by which ERC-Exos loaded with siSLAMF6 can alleviate allogeneic transplant rejection.</p><p><strong>Methods: </strong>C57BL/6 mouse recipients of BALB/c mouse kidney transplants were randomly divided into four groups and treated with exosomes. The graft pathology was evaluated by H&E staining. Splenic and transplanted heart immune cell populations were analyzed by flow cytometry. Recipient serum cytokine profiles were determined by enzyme-linked immunosorbent assay (ELISA). The proliferation and differentiation capacity of CD4⁺ T cell populations were evaluated in vitro. The α-2,6-sialylation levels in the CD4⁺ T cells were determined by SNA blotting.</p><p><strong>Results: </strong>In vivo, mice treated with ERC-siSLAMF6 Exo achieved significantly prolonged allograft survival. The serum cytokine profiles of the recipients were significantly altered in the ERC-siSLAMF6 Exo-treated recipients. In vitro, we found that ERC-siSLAMF6-Exo considerably downregulated α-2,6-sialyltransferase (ST6GAL1) expression in CD4⁺ T cells, and significantly reduced α-2,6-sialylation levels. Through desialylation, ERC-siSLAMF6 Exo therapy significantly decreased CD4⁺ T cell proliferation and inhibited CD4⁺ T cell differentiation into Th1 and Th17 cells while promoting regulatory T cell (Treg) differentiation.</p><p><strong>Conclusions: </strong>Our study indicated that ERC-Exos loaded with siSLAMF6 reduce the amount of sialic acid connected to α-2,6 at the end of the N-glycan chain on the CD4⁺ T cell surface, increase the number of therapeutic exosomes endocytosed into CD4⁺ T cells, and inhibit the activation of T cell receptor signaling pathways, which prolongs allograft survival. This study confirms the feasibility of using ERC-Exos as natural carriers combined with gene therapy, which could be used as a potential therapeutic strategy to alleviate allograft rejection.</p>","PeriodicalId":9688,"journal":{"name":"Cellular & Molecular Biology Letters","volume":null,"pages":null},"PeriodicalIF":9.2,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11443917/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142361189","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role and therapeutic potential of itaconate in lung disease.","authors":"Ruyuan He, Yifan Zuo, Ke Yi, Bohao Liu, Congkuan Song, Ning Li, Qing Geng","doi":"10.1186/s11658-024-00642-1","DOIUrl":"10.1186/s11658-024-00642-1","url":null,"abstract":"<p><p>Lung diseases triggered by endogenous or exogenous factors have become a major concern, with high morbidity and mortality rates, especially after the coronavirus disease 2019 (COVID-19) pandemic. Inflammation and an over-activated immune system can lead to a cytokine cascade, resulting in lung dysfunction and injury. Itaconate, a metabolite produced by macrophages, has been reported as an effective anti-inflammatory and anti-oxidative stress agent with significant potential in regulating immunometabolism. As a naturally occurring metabolite in immune cells, itaconate has been identified as a potential therapeutic target in lung diseases through its role in regulating inflammation and immunometabolism. This review focuses on the origin, regulation, and function of itaconate in lung diseases, and briefly discusses its therapeutic potential.</p>","PeriodicalId":9688,"journal":{"name":"Cellular & Molecular Biology Letters","volume":null,"pages":null},"PeriodicalIF":9.2,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11445945/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142361190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel protein SPECC1-415aa encoded by N6-methyladenosine modified circSPECC1 regulates the sensitivity of glioblastoma to TMZ.","authors":"Cheng Wei, Dazhao Peng, Boyuan Jing, Bo Wang, Zesheng Li, Runze Yu, Shu Zhang, Jinquan Cai, Zhenyu Zhang, Jianning Zhang, Lei Han","doi":"10.1186/s11658-024-00644-z","DOIUrl":"10.1186/s11658-024-00644-z","url":null,"abstract":"<p><strong>Background: </strong>Circular RNAs (circRNAs) can influence a variety of biological functions and act as a significant role in the progression and recurrence of glioblastoma (GBM). However, few coding circRNAs have been discovered in cancer, and their role in GBM is still unknown. The aim of this study was to identify coding circRNAs and explore their potential roles in the progression and recurrence of GBM.</p><p><strong>Methods: </strong>CircSPECC1 was screened via circRNAs microarray of primary and recurrent GBM samples. To ascertain the characteristics and coding ability of circSPECC1, we conducted a number of experiments. Afterward, through in vivo and in vitro experiments, we investigated the biological functions of circSPECC1 and its encoded novel protein (SPECC1-415aa) in GBM, as well as their effects on TMZ sensitivity.</p><p><strong>Results: </strong>By analyzing primary and recurrent GBM samples via circRNAs microarray, circSPECC1 was found to be a downregulated circRNA with coding potential in recurrent GBM compared with primary GBM. CircSPECC1 suppressed the proliferation, migration, invasion, and colony formation abilities of GBM cells by encoding a new protein known as SPECC1-415aa. CircSPECC1 restored TMZ sensitivity in TMZ-resistant GBM cells by encoding the new protein SPECC1-415aa. The m⁶A reader protein IGF2BP1 can bind to circSPECC1 to promote its expression and stability. Mechanistically, SPECC1-415aa can bind to ANXA2 and competitively inhibit the binding of ANXA2 to EGFR, thus resulting in the inhibition of the phosphorylation of EGFR (Tyr845) and its downstream pathway protein AKT (Ser473). In vivo experiments showed that the overexpression of circSPECC1 could combine with TMZ to treat TMZ-resistant GBM, thereby restoring the sensitivity of TMZ-resistant GBM to TMZ.</p><p><strong>Conclusions: </strong>CircSPECC1 was downregulated in recurrent GBM compared with primary GBM. The m6A reader protein IGF2BP1 could promote the expression and stability of circSPECC1. The sequence of SPECC1-415aa, which is encoded by circSPECC1, can inhibit the binding of ANXA2 to EGFR by competitively binding to ANXA2 and inhibiting the phosphorylation of EGFR and AKT, thereby restoring the sensitivity of TMZ-resistant GBM cells to TMZ.</p>","PeriodicalId":9688,"journal":{"name":"Cellular & Molecular Biology Letters","volume":null,"pages":null},"PeriodicalIF":9.2,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11429730/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142342433","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tetraspanin 3 promotes NSCLC cell proliferation via regulation of β1 integrin intracellular recycling.","authors":"Yao Zhang, Chenglong Wang, Yitong Xu, Hongbo Su","doi":"10.1186/s11658-024-00639-w","DOIUrl":"10.1186/s11658-024-00639-w","url":null,"abstract":"<p><strong>Background: </strong>The involvement of tetraspanins in cancer development has been widely implicated. In this study, the function and molecular mechanisms of tetraspanin 3 (TSPAN3) in non-small cell lung cancer (NSCLC) cells were explored.</p><p><strong>Methods: </strong>Tissue samples from patients diagnosed with NSCLC were analyzed by immunohistochemistry, western blotting, and real-time polymerase chain reaction (PCR) to indicate the involvement of TSPAN3 in cancer progression. In the meantime, we also performed exhaustive mechanistic studies using A549 and H460 cells in vitro through a variety of methods including western blotting, real-time PCR, immunofluorescent staining, coimmunoprecipitation, cell proliferation assay, and nocodazole (NZ) washout assay. Proper statistical analysis was implemented wherever necessary in this study.</p><p><strong>Results: </strong>TSPAN3 was found to be highly expressed in lung cancer cells and tissues. Moreover, high levels of TSPAN3 positively correlated with poor differentiation, lymph node involvement, advanced pathological tumor-node-metastasis stage, and poor prognosis in patients with NSCLC. TSPAN3 showed potential to promote the proliferation of NSCLC cells in vitro and in vivo. Specifically, TSPAN3 was found to interact with β1 integrin via the LEL domain, thereby facilitating the sorting of β1 integrin into Rab11a endosomes and promoting β1 integrin recycling and upregulation.</p><p><strong>Conclusions: </strong>Our findings reveal TSPAN3 may represent a potentially valuable therapeutic target for NSCLC.</p>","PeriodicalId":9688,"journal":{"name":"Cellular & Molecular Biology Letters","volume":null,"pages":null},"PeriodicalIF":9.2,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11428915/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142342435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}