Journal of Cell Communication and Signaling最新文献

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Cellular communication network 1 promotes CASP2 mRNA expression but suppresses its protein translation in esophageal adenocarcinoma 细胞通讯网络 1 促进食管腺癌中 CASP2 mRNA 的表达,但抑制其蛋白翻译
IF 3.6 3区 生物学
Journal of Cell Communication and Signaling Pub Date : 2024-07-17 DOI: 10.1002/ccs3.12046
Ruize Xu, Zhenyu Jiang, Xianmei Meng, Lingling Xing, Wula Aladan, Baoxing Chi, Tong Dang, Jianyuan Chai
{"title":"Cellular communication network 1 promotes CASP2 mRNA expression but suppresses its protein translation in esophageal adenocarcinoma","authors":"Ruize Xu,&nbsp;Zhenyu Jiang,&nbsp;Xianmei Meng,&nbsp;Lingling Xing,&nbsp;Wula Aladan,&nbsp;Baoxing Chi,&nbsp;Tong Dang,&nbsp;Jianyuan Chai","doi":"10.1002/ccs3.12046","DOIUrl":"10.1002/ccs3.12046","url":null,"abstract":"<p>Induction of apoptosis in tumor cells is one of the best ways to cure cancer. While most apoptosis requires a chain of caspase activation, CASP2 can do this all by itself. The matricellular protein cellular communication network 1 (CCN1) is known for supporting some cancer growth but suppressing others. Esophageal adenocarcinoma (EAC) belongs to the latter. CCN1 is capable of inducing TRAIL-mediated apoptosis in EAC cells. This study found that CCN1 upregulated CASP2 transcription but not its translation in EAC cells because, on one hand, CCN1 downregulated p16 and p21, which increased RB1 phosphorylation allowing E2F1 to transcribe more CASP2 mRNA, on the other hand, CCN1 also upregulated HuR, which is bound to CASP2 mRNA species and blocked its protein translation. As a result, CASP2 contributed nothing to CCN1-induced EAC cell apoptosis. On the contrary, CCN1 promoted CASP3, not only in its transcription but also in its translation and activation, which established the basis for CCN1-induced EAC cell apoptosis.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"18 3","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.12046","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141828146","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}
引用次数: 0
Retraction: A network map of cytoskeleton-associated protein 4 (CKAP4) mediated signaling pathway in cancer 撤回:癌症中细胞骨架相关蛋白 4 (CKAP4) 介导的信号通路网络图
IF 3.6 3区 生物学
Journal of Cell Communication and Signaling Pub Date : 2024-07-11 DOI: 10.1002/ccs3.12043
{"title":"Retraction: A network map of cytoskeleton-associated protein 4 (CKAP4) mediated signaling pathway in cancer","authors":"","doi":"10.1002/ccs3.12043","DOIUrl":"https://doi.org/10.1002/ccs3.12043","url":null,"abstract":"<p>Retraction: Suchitha, G. P., Balaya, R. D. A, Raju, R., Prasad, T. S. K, Dagamajalu, S. (2023) A network map of cytoskeleton-associated protein 4 (CKAP4) mediated signaling pathway in cancer. <i>Journal of Cell Communication and Signaling</i>, <i>17</i>: 1097–1104. https://doi.org/10.1007/s12079-023-00739-w.</p><p>The above article, published online on March 21, 2023 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors, journal Editor-in-Chief Bernard Perbal and John Wiley &amp; Sons, Ltd. The retraction has been agreed following a report by a third party which described methodological errors in the published article. The authors have confirmed that the article contains annotation errors caused by the same alternate names for two different proteins. The editor and authors agree that the conclusions are fundamentally impacted by this error and that the article must be retracted.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"18 3","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.12043","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142273078","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}
引用次数: 0
Gastrokine 1 transferred by gastric cancer exosomes inhibits growth and invasion of gastric cancer cells in vitro and in vivo 胃癌外泌体转移的胃泌素 1 在体外和体内抑制胃癌细胞的生长和侵袭
IF 3.6 3区 生物学
Journal of Cell Communication and Signaling Pub Date : 2024-07-07 DOI: 10.1002/ccs3.12044
Lingling Tian, Li Tang, Xu Li, Liuye Huang
{"title":"Gastrokine 1 transferred by gastric cancer exosomes inhibits growth and invasion of gastric cancer cells in vitro and in vivo","authors":"Lingling Tian,&nbsp;Li Tang,&nbsp;Xu Li,&nbsp;Liuye Huang","doi":"10.1002/ccs3.12044","DOIUrl":"10.1002/ccs3.12044","url":null,"abstract":"<p>In gastric cancer, gastrokine 1 (GKN1) is a potential theragnostic marker while the related mechanisms remain elusive. Exosomes mediate intercellular communications via transferring various molecules, yet there are limited research studies on the specific cargos of gastric cancer exosomes and the associated mechanisms in this disease. In the present study, AGS and N87-C cells were transfected with an overexpressed GKN1 plasmid, followed by extraction of exosomes. The study utilized gastric cancer cell lines and a xenograft mouse model to investigate the functional significance of exosomal GKN1. Cell proliferation, metastasis, and apoptosis were assessed through CCK-8, Transwell, and flow cytometry assays, respectively. The study further explored the mechanism of exosomal GKN1 and its interaction with the PI3K/AKT/mTOR signaling pathways, including immunofluorescence and western blot analyses. Exosomal GKN1 was observed to suppress cell proliferation and invasion while enhancing apoptosis. This effect was attributed to the modulation of key proteins involved in cellular processes, including Ki-67, MMP-9, Bcl-2, Bax, caspase-3, and caspase-9, ultimately impacting the PI3K/AKT/mTOR signaling pathway. The findings suggest that exosomal GKN1 exerts inhibitory effects on gastric cancer cell growth and invasion through the regulation of the PI3K/AKT/mTOR signaling cascade, both in experimental cell cultures and animal models.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"18 3","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.12044","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141670714","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}
引用次数: 0
Hypoxia drives CBR4 down-regulation promotes gastroenteropancreatic neuroendocrine tumors via activation mammalian target of rapamycin mediated by fatty acid synthase 缺氧通过激活脂肪酸合成酶介导的哺乳动物雷帕霉素靶标,促使 CBR4 下调,从而促进胃肠胰神经内分泌肿瘤的发生
IF 3.6 3区 生物学
Journal of Cell Communication and Signaling Pub Date : 2024-06-22 DOI: 10.1002/ccs3.12041
Mujie Ye, Lin Xu, Feiyu Lu, Lingyi Chen, Chunhua Hu, Jinhao Chen, Bingyan Xue, Danyang Gu, Ruitong Xu, Yanling Xu, Ping Yu, Yan Wang, Ye Tian, Guoqin Zhu, Qiyun Tang
{"title":"Hypoxia drives CBR4 down-regulation promotes gastroenteropancreatic neuroendocrine tumors via activation mammalian target of rapamycin mediated by fatty acid synthase","authors":"Mujie Ye,&nbsp;Lin Xu,&nbsp;Feiyu Lu,&nbsp;Lingyi Chen,&nbsp;Chunhua Hu,&nbsp;Jinhao Chen,&nbsp;Bingyan Xue,&nbsp;Danyang Gu,&nbsp;Ruitong Xu,&nbsp;Yanling Xu,&nbsp;Ping Yu,&nbsp;Yan Wang,&nbsp;Ye Tian,&nbsp;Guoqin Zhu,&nbsp;Qiyun Tang","doi":"10.1002/ccs3.12041","DOIUrl":"https://doi.org/10.1002/ccs3.12041","url":null,"abstract":"<p>Hypoxia has been highly proven a hallmark of tumor micro-environment, promoting the malignant phenotypes, playing a crucial role from tumor initiation, progression, invasion, and intravasation to metastatic dissemination and outgrowth. Increasing evidence also showed that hypoxia mediated the abnormal lipid metabolism in cancer by regulating various oncogenic signal pathways. However, it is still unclear but attractive how hypoxia specifically functioned and changed the condition of the tumor micro-environment. In present study, we find that hypoxia promoted the methylation degree of <i>CBR4</i> promoter region thus downgraded the expression of <i>CBR4</i>, which promoted GEP-NETs progression and increased the sensitivity of GEP-NETs cells to everolimus. Further, CBR4 interacted with fatty acid synthase (FASN), displaying a down-regulation of <i>FASN</i> by activating the ubiquitin proteasome pathway and suppressed mTOR signaling. Overall, our results uncovers the <i>CBR4/FASN/mTOR</i> axis as a mechanism for tumor development and inspires us a new molecular guide for the therapeutic strategies for GEP-NETs treatment.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"18 3","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.12041","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142273287","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}
引用次数: 0
The signaling pathways in obesity-related complications 肥胖相关并发症的信号通路
IF 3.6 3区 生物学
Journal of Cell Communication and Signaling Pub Date : 2024-06-07 DOI: 10.1002/ccs3.12039
Preethi Chandrasekaran, Ralf Weiskirchen
{"title":"The signaling pathways in obesity-related complications","authors":"Preethi Chandrasekaran,&nbsp;Ralf Weiskirchen","doi":"10.1002/ccs3.12039","DOIUrl":"10.1002/ccs3.12039","url":null,"abstract":"<p>Obesity, a rapidly expanding epidemic worldwide, is known to exacerbate many medical conditions, making it a significant factor in multiple diseases and their associated complications. This threatening epidemic is linked to various harmful conditions such as type 2 diabetes mellitus, hypertension, metabolic dysfunction-associated steatotic liver disease, polycystic ovary syndrome, cardiovascular diseases (CVDs), dyslipidemia, and cancer. The rise in urbanization and sedentary lifestyles creates an environment that fosters obesity, leading to both psychosocial and medical complications. To identify individuals at risk and ensure timely treatment, it is crucial to have a better understanding of the pathophysiology of obesity and its comorbidities. This comprehensive review highlights the relationship between obesity and obesity-associated complications, including type 2 diabetes, hypertension, (CVDs), dyslipidemia, polycystic ovary syndrome, metabolic dysfunction-associated steatotic liver disease, gastrointestinal complications, and obstructive sleep apnea. It also explores the potential mechanisms underlying these associations. A thorough analysis of the interplay between obesity and its associated complications is vital in developing effective therapeutic strategies to combat the exponential increase in global obesity rates and mitigate the deadly consequences of this polygenic condition.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"18 2","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.12039","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141374510","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}
引用次数: 0
Enoyl coenzyme a hydratase 1 attenuates aortic valve calcification by suppressing Runx2 via Wnt5a/Ca2+ pathway 通过Wnt5a/Ca2+途径抑制Runx2,烯酰辅酶a水解酶1可减轻主动脉瓣钙化。
IF 3.6 3区 生物学
Journal of Cell Communication and Signaling Pub Date : 2024-05-31 DOI: 10.1002/ccs3.12038
Caijun Rao, Baoqing Liu, Haojie Qin, Zhipeng Du
{"title":"Enoyl coenzyme a hydratase 1 attenuates aortic valve calcification by suppressing Runx2 via Wnt5a/Ca2+ pathway","authors":"Caijun Rao,&nbsp;Baoqing Liu,&nbsp;Haojie Qin,&nbsp;Zhipeng Du","doi":"10.1002/ccs3.12038","DOIUrl":"10.1002/ccs3.12038","url":null,"abstract":"<p>The morbidity and death rates of calcified aortic valves|calcific aortic valve (CAV) disease (CAVD) remain high for its limited therapeutic choices. Here, we investigated the function, therapeutic potential, and putative mechanisms of Enoyl coenzyme A hydratase 1 (ECH1) in CAVD by various in vitro and in vivo experiments. Single-cell sequencing revealed that ECH1 was predominantly expressed in valve interstitial cells and was significantly reduced in CAVs. Overexpression of ECH1 reduced aortic valve calcification in ApoE<sup>−/−</sup> mice treated with high cholesterol diet, while ECH1 silencing had the reverse effect. We also identified Wnt5a, a noncanonical Wnt ligand, was also altered when ECH1 expression was modulated. Mechanistically, we found that ECH1 exerted anti-calcific actions through suppressing Wnt signaling, since CHIR99021, a Wnt agonist, may significantly lessen the protective impact of ECH1 overexpression on the development of valve calcification. ChIP and luciferase assays all showed that ECH1 overexpression prevented Runx2 binding to its downstream gene promoters (osteopontin and osteocalcin), while CHIR99021 neutralized this protective effect. Collectively, our findings reveal a previously unrecognized mechanism of ECH1-Wnt5a/Ca<sup>2+</sup> regulation in CAVD, implying that targeting ECH1 may be a potential therapeutic strategy to prevent CAVD development.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"18 2","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11208118/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141468303","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}
引用次数: 0
LncRNA Snhg12/IGFBP3 axis is involved in liver fibrosis by promoting the proliferation and activation of mouse hepatic stellate cells LncRNA Snhg12/IGFBP3轴通过促进小鼠肝星状细胞的增殖和活化参与肝纤维化。
IF 3.6 3区 生物学
Journal of Cell Communication and Signaling Pub Date : 2024-05-28 DOI: 10.1002/ccs3.12033
Jingmao Liao, Qi Yuan, Lidan Luo, Xiaoxuan Hu, Zhengzheng Li, Zheng Zhang
{"title":"LncRNA Snhg12/IGFBP3 axis is involved in liver fibrosis by promoting the proliferation and activation of mouse hepatic stellate cells","authors":"Jingmao Liao,&nbsp;Qi Yuan,&nbsp;Lidan Luo,&nbsp;Xiaoxuan Hu,&nbsp;Zhengzheng Li,&nbsp;Zheng Zhang","doi":"10.1002/ccs3.12033","DOIUrl":"10.1002/ccs3.12033","url":null,"abstract":"<p>Liver fibrosis is a persistent damage repair response triggered by various injury factors, which leads to an abnormal accumulation of extracellular matrix within liver tissue samples. The current clinical treatment of liver fibrosis is currently ineffective; therefore, elucidating the mechanism of liver fibrogenesis is of significant importance. Herein, the function and related mechanisms of lncRNA <i>Snhg12</i> within hepatic fibrosis were investigated. <i>Snhg12</i> expression was shown to be increased in mouse hepatic fibrotic tissue samples, and <i>Snhg12</i> knockdown suppressed hepatic pathological injury and down-regulated the expression levels of fibrosis-associated proteins. Mechanistically, <i>Snhg12</i> played a role in the early activation of mouse hepatic stellate cells (mHSCs) based on bioinformatics analysis, and <i>Snhg12</i> was positively correlated with Igfbp3 expression. Further experimental results demonstrated that <i>Snhg12</i> knockdown impeded mHSCs proliferation and activation and also downregulated the protein expression of Igfbp3. <i>Snhg12</i> could interact with IGFBP3 and boost its protein stability, and overexpression of <i>Igfbp3</i> partially reversed the inhibition of mHSCsproliferation and activation by the knockdown of <i>Snhg12</i>. In conclusion, LncRNA <i>Snhg12</i> mediates liver fibrosis by targeting IGFBP3 and promoting its protein stability, thereby promoting mHSC proliferation and activation. <i>Snhg12</i> has been identified as an underlying target for treating liver fibrosis.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"18 2","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11208121/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141468304","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}
引用次数: 0
POSTN knockdown suppresses IL-1β-induced inflammation and apoptosis of nucleus pulposus cells via inhibiting the NF-κB pathway and alleviates intervertebral disc degeneration 通过抑制 NF-κB 通路,敲除 POSTN 可抑制 IL-1β 诱导的髓核细胞炎症和凋亡,缓解椎间盘退变
IF 3.6 3区 生物学
Journal of Cell Communication and Signaling Pub Date : 2024-05-07 DOI: 10.1002/ccs3.12030
Zhaoheng Wang, Daxue Zhu, Fengguang Yang, Haiwei Chen, Jihe Kang, Wenzhao Liu, Aixin Lin, Xuewen Kang
{"title":"POSTN knockdown suppresses IL-1β-induced inflammation and apoptosis of nucleus pulposus cells via inhibiting the NF-κB pathway and alleviates intervertebral disc degeneration","authors":"Zhaoheng Wang,&nbsp;Daxue Zhu,&nbsp;Fengguang Yang,&nbsp;Haiwei Chen,&nbsp;Jihe Kang,&nbsp;Wenzhao Liu,&nbsp;Aixin Lin,&nbsp;Xuewen Kang","doi":"10.1002/ccs3.12030","DOIUrl":"10.1002/ccs3.12030","url":null,"abstract":"<p>The aim of this study is to investigate the effects of POSTN on IL-1β induced inflammation, apoptosis, NF-κB pathway and intervertebral disc degeneration (IVDD) in Nucleus pulposus (NP) cells (NPCs). NP tissue samples with different Pfirrmann grades were collected from patients with different degrees of IVDD. Western blot and immunohistochemical staining were used to compare the expression of POSTN protein in NP tissues. Using the IL-1β-induced IVDD model, NPCs were transfected with lentivirus-coated si-POSTN to down-regulate the expression of POSTN and treated with CU-T12-9 to evaluate the involvement of NF-κB pathway. Western blot, immunofluorescence, and TUNEL staining were used to detect the expression changes of inflammation, apoptosis and NF-κB pathway-related proteins in NPCs. To investigate the role of POSTN in vivo, a rat IVDD model was established by needle puncture of the intervertebral disc. Rats were injected with lentivirus-coated si-POSTN, and H&amp;E staining and immunohistochemical staining were performed. POSTN expression is positively correlated with the severity of IVDD in human. POSTN expression was significantly increased in the IL-1β-induced NPCs degeneration model. Downregulation of POSTN protects NPCs from IL-1β-induced inflammation and apoptosis. CU-T12-9 treatment reversed the protective effect of si-POSTN on NPCs. Furthermore, lentivirus-coated si-POSTN injection partially reversed NP tissue damage in the IVDD model in vivo. POSTN knockdown reduces inflammation and apoptosis of NPCs by inhibiting NF-κB pathway, and ultimately prevents IVDD. Therefore, POSTN may be an effective target for the treatment of IVDD.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"18 2","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.12030","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141003618","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}
引用次数: 0
TM4SF1 is a molecular facilitator that distributes cargo proteins intracellularly in endothelial cells in support of blood vessel formation TM4SF1 是一种分子促进剂,它能在细胞内皮细胞中分配货物蛋白,支持血管的形成
IF 3.6 3区 生物学
Journal of Cell Communication and Signaling Pub Date : 2024-05-07 DOI: 10.1002/ccs3.12031
Chi-Iou Lin, Anne Merley, Shou-Ching S. Jaminet
{"title":"TM4SF1 is a molecular facilitator that distributes cargo proteins intracellularly in endothelial cells in support of blood vessel formation","authors":"Chi-Iou Lin,&nbsp;Anne Merley,&nbsp;Shou-Ching S. Jaminet","doi":"10.1002/ccs3.12031","DOIUrl":"10.1002/ccs3.12031","url":null,"abstract":"<p>Transmembrane-4 L-six family member-1 (TM4SF1) is an atypical tetraspanin that is highly and selectively expressed in proliferating endothelial cells and plays an essential role in blood vessel development. TM4SF1 forms clusters on the cell surface called TMED (<span>TM</span>4SF1-<span>e</span>nriched micro<span>d</span>omains) and recruits other proteins that internalize along with TM4SF1 via microtubules to intracellular locations including the nucleus. We report here that tumor growth and wound healing are inhibited in <i>Tm4sf1</i>-heterozygous mice. Investigating the mechanisms of TM4SF1 activity, we show that 12 out of 18 signaling molecules examined are recruited to TMED on the surface of cultured human umbilical vein endothelial cells (HUVEC) and internalize along with TMED; notable among them are PLCγ and HDAC6. When TM4SF1 is knocked down in HUVEC, microtubules are heavily acetylated despite normal levels of HDAC6 protein, and, despite normal levels of VEGFR2, are unable to proliferate. Together, our studies indicate that pathological angiogenesis is inhibited when levels of TM4SF1 are reduced as in <i>Tm4sf1</i>-heterozygous mice; a likely mechanism is that TM4SF1 regulates the intracellular distribution of signaling molecules necessary for endothelial cell proliferation and migration.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"18 2","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.12031","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141004863","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}
引用次数: 0
CircORC2 promoted proliferation and inhibited the sensitivity of osteosarcoma cell lines to cisplatin by regulating the miR-485-3p/TRIM2 axis CircORC2 通过调控 miR-485-3p/TRIM2 轴促进骨肉瘤细胞株的增殖并抑制其对顺铂的敏感性。
IF 3.6 3区 生物学
Journal of Cell Communication and Signaling Pub Date : 2024-04-25 DOI: 10.1002/ccs3.12029
Tianhua Chen, Zuyang Zhang, Chao Tian, Yuchao Feng, Xiaojie He, Liangdong Jiang
{"title":"CircORC2 promoted proliferation and inhibited the sensitivity of osteosarcoma cell lines to cisplatin by regulating the miR-485-3p/TRIM2 axis","authors":"Tianhua Chen,&nbsp;Zuyang Zhang,&nbsp;Chao Tian,&nbsp;Yuchao Feng,&nbsp;Xiaojie He,&nbsp;Liangdong Jiang","doi":"10.1002/ccs3.12029","DOIUrl":"10.1002/ccs3.12029","url":null,"abstract":"<p>Resistance to chemotherapy leads to poor prognosis for osteosarcoma (OS) patients. However, due to the high metastasis of tumor and the decrease in sensitivity of tumor cells to cisplatin (DDP), the 5-year survival rate of OS patients is still unsatisfactory. This study explored a mechanism for improving the sensitivity of OS cells to DDP. A DDP-resistant OS cell model was established, and we have found that circORC2 and TRIM2 were upregulated in DDP-resistant OS cells, but miR-485-3p was downregulated. The cell viability and proliferation of the OS cells decreased gradually with the increase of DDP dose, but a gradual increase in apoptosis was noted. CircORC2 promoted OS cell proliferation and DDP resistance and upregulated TRIM2 expression by targeting miR-485-3p. Functionally, circORC2 downregulated miR-485-3p to promote OS cell proliferation and inhibit DDP sensitivity. Additionally, it promoted cell proliferation and inhibited the sensitivity of DDP by regulating the miR-485-3p/TRIM2 axis. In conclusion, circORC2 promoted cell proliferation and inhibited the DDP sensitivity in OS cells via the miR-485-3p/TRIM2 axis. These findings indicated the role of circORC2 in regulating the sensitivity of OS cells to DDP.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"18 2","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11208123/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141468302","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}
引用次数: 0
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