Journal of Cell Communication and Signaling最新文献_第2页

Tert-butyl hydroperoxide induces trabecular meshwork cells injury through ferroptotic cell death 叔丁基过氧化氢通过铁性细胞死亡诱导小梁网细胞损伤

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2024-08-28 DOI: 10.1002/ccs3.12050

Xuejing Yan, Qian Liu, Shen Wu, Xiaowei Fan, Yufei Teng, Ningli Wang, Jingxue Zhang

{"title":"Tert-butyl hydroperoxide induces trabecular meshwork cells injury through ferroptotic cell death","authors":"Xuejing Yan, Qian Liu, Shen Wu, Xiaowei Fan, Yufei Teng, Ningli Wang, Jingxue Zhang","doi":"10.1002/ccs3.12050","DOIUrl":"https://doi.org/10.1002/ccs3.12050","url":null,"abstract":"Trabecular meshwork (TM) tissue has a crucial role in regulating aqueous humor circulation in the eye, thus maintaining normal intraocular pressure (IOP). TM dysfunction causes IOP elevation, which leads to glaucoma. To investigate biological changes in TM tissue in patients with glaucoma, we analyzed the mRNA expression microarray dataset, GSE27276. Gene ontology analysis indicated that redox microenvironment imbalance is among the main changes of TM tissue in patients with glaucoma. Subsequently, we induced oxidative stress in TM cells using the tert-butyl hydroperoxide (tBHP) treatment, to generate in vivo and in vitro models, and conducted mRNA sequencing to identify genes with critical roles in maintaining the redox microenvironment balance. We found that the tBHP caused TM dysfunction in vivo, characterized by aqueous humor circulation resistance, IOP elevation, and TM cell death. Further, Kyoto Encyclopedia of Genes and Genomes pathway analysis showed that ferroptosis signaling was enriched in tBHP-treated TM cells. Consistently, in vitro analyses showed that levels of reactive oxygen species, ferric ion, and malondialdehyde were increased after the tBHP treatment, indicating TM cell ferroptosis. Furthermore, inhibiting ferroptosis alleviated tBHP-induced TM cell injury. This study provides new insights suggesting that inhibition of ferroptosis has potential as a treatment for glaucoma.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"18 3","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.12050","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142273204","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

Association for research on biosignaling and communication first world conference on cellular communication and signaling 生物信号和通信研究协会第一届世界细胞通信和信号会议

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2024-08-13 DOI: 10.1002/ccs3.12048

Bernard Perbal, Ralf Weiskirchen

引用次数: 0

Report on the 12th international workshop on the CCN family of genes, Oslo, June 20–23, 2024 第 12 届 CCN 基因家族国际研讨会报告，奥斯陆，2024 年 6 月 20-23 日

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2024-08-13 DOI: 10.1002/ccs3.12049

Håvard Attramadal, Ralf Weiskirchen, Bernard Perbal

{"title":"Report on the 12th international workshop on the CCN family of genes, Oslo, June 20–23, 2024","authors":"Håvard Attramadal, Ralf Weiskirchen, Bernard Perbal","doi":"10.1002/ccs3.12049","DOIUrl":"https://doi.org/10.1002/ccs3.12049","url":null,"abstract":"The 12th international workshop on the CCN family of genes took place at the Scandic Holmenkollen Park Hotel in Oslo, Norway from June 20–23, 2024. In 2024, it was the second time, following the Nice meeting in 2022, that the scientific topics were expanded to include additional cellular signaling and communication pathways of interest to the CCN Society members, as suggested by Bernard Perbal in 2019. The 12th international CCN workshop, organized by Håvard Attramadal and Vivi T. Monsen, along with co-organizers Bernard and Annick Perbal, was given the subtitle “Cell-matrix Communication and Functions in Health and Disease” to encompass the broader scope of this meeting. The five scientific sessions covered various topics: Extracellular Matrix Proteins in Cell Communication and Signaling (Chaired by Brahim Chaqour and Vivi T. Monsen), Vascular Development and Pathophysiology (Chaired by Lester F. Lau and Håvard Attramadal), Mechanisms of Diseases (Chaired by George Bou-Gharios and Satoshi Kubota), Tissue Development and Homeostasis (Chaired by Blandine Poulet and Bernard Perbal), and Mechanisms of Disease: Cancer and the Matrix (Chaired by Stephen M. Twigg and Raymond B. Birge). The 2024 ICCNS Award was presented to Katia Scotlandi during the last session (Chaired by Bernard Perbal) before Håvard Attramadal presented the conclusion of the workshop.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"18 3","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.12049","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142273148","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

CD99 contributes to the EWS::FLI1 transcriptome by specifically affecting FOXM1-targets involved in the G2/M cell cycle phase, thus influencing the Ewing sarcoma genetic landscape CD99 通过特异性影响参与 G2/M 细胞周期阶段的 FOXM1 靶点，从而影响尤文肉瘤的基因格局，为 EWS::FLI1 转录组做出了贡献

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2024-08-02 DOI: 10.1002/ccs3.12047

Michela Pasello, Maria Antonella Laginestra, Maria Cristina Manara, Lorena Landuzzi, Francesca Ruzzi, Margherita Maioli, Evelin Pellegrini, Alessandra De Feo, Pier-Luigi Lollini, Katia Scotlandi

{"title":"CD99 contributes to the EWS::FLI1 transcriptome by specifically affecting FOXM1-targets involved in the G2/M cell cycle phase, thus influencing the Ewing sarcoma genetic landscape","authors":"Michela Pasello, Maria Antonella Laginestra, Maria Cristina Manara, Lorena Landuzzi, Francesca Ruzzi, Margherita Maioli, Evelin Pellegrini, Alessandra De Feo, Pier-Luigi Lollini, Katia Scotlandi","doi":"10.1002/ccs3.12047","DOIUrl":"https://doi.org/10.1002/ccs3.12047","url":null,"abstract":"Ewing sarcoma (EwS), a highly aggressive malignancy affecting children and young adults, is primarily driven by a distinctive oncogenic fusion, the EWSR1-ETS, whose activity is a key source of epigenetic and clinical heterogeneity. CD99 is constantly present in EwS cells, known to modulate the EwS genetic profile and tumor malignancy. However, the relevance of CD99 alone, or in association with EWSR1-ETS chimeras, is poorly understood. We explored the dynamic relationship between CD99 and EWS::FLI1, the main fusion observed in EwS, by means of model systems with inducible expression of either molecule. The transcriptomic dynamics of cells with or without expression of EWS::FLI1 or CD99 were analyzed and correlated with tumor cell growth. The CD99-associated EwS gene profile was found to have commonalities with the profile induced by EWS::FLI1, but also peculiar differences. Both EWS::FLI1 and CD99 are regulated targets of the DREAM complex, but the CD99 expression specifically impacted genes that are the targets of FOXM1 and are involved in the setting of the G2/M phase of the cell cycle. Most CD99-regulated FOXM1-targeted genes were found to correlate with bad prognosis in two public clinical datasets (R2 platform), further supporting the clinical relevance of CD99-mediated regulation of EwS gene expression.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"18 3","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.12047","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142273046","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

Elevated reactive aggression in forebrain-specific Ccn2 knockout mice 前脑特异性 Ccn2 基因敲除小鼠的反应性攻击性增强

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2024-07-20 DOI: 10.1002/ccs3.12040

Ho-Ching Chang, Chi-Hou Ng, Yu-Fu Chen, Yu-Chun Wang, I-Shing Yu, Lukas Jyuhn-Hsiarn Lee, Li-Jen Lee, Kuang-Yung Lee

{"title":"Elevated reactive aggression in forebrain-specific Ccn2 knockout mice","authors":"Ho-Ching Chang, Chi-Hou Ng, Yu-Fu Chen, Yu-Chun Wang, I-Shing Yu, Lukas Jyuhn-Hsiarn Lee, Li-Jen Lee, Kuang-Yung Lee","doi":"10.1002/ccs3.12040","DOIUrl":"10.1002/ccs3.12040","url":null,"abstract":"Cellular communication network factor 2 (CCN2) is a matricellular protein that plays important roles in connective tissue. CCN2 is also expressed in the nervous system; however, its role is still unclear. To explore CCN2 function in the brain, we generated forebrain-specific Ccn2 knockout (FbCcn2 KO) mice. In this study, we examined the behavioral phenotypes of FbCcn2KO mice. Male mice lacking CCN2 in the forebrain exhibited normal locomotion, sensorimotor gating, and social behaviors but signs of anxiety and elevated reactive aggression. We checked the c-fos expression in aggression-related brain regions following the resident-intruder task (RIT), an aggression test. RIT-induced c-fos levels in the medial amygdala (MeA) were higher in FbCcn2−/− mice as compared to controls. However, in the prefrontal cortex, RIT-induced c-fos levels in FbCcn2−/− mice were lower than controls. Our results suggested in male mice lacking CCN2 in the olfaction-related regions, olfactory social cues elicit greater signals in the MeA, resulting in greater reactive aggression in the RIT. Further, lacking CCN2 in the prefrontal cortex, the major area related to inhibitory control and emotion regulation, may lead to signs of anxiety and the failure to suppress aggressive behaviors. Our model is useful in elaborating the mechanism underlying reactive aggression and therapeutic strategies.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"18 3","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.12040","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141820678","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

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, Zhenyu Jiang, Xianmei Meng, Lingling Xing, Wula Aladan, Baoxing Chi, Tong Dang, Jianyuan Chai","doi":"10.1002/ccs3.12046","DOIUrl":"10.1002/ccs3.12046","url":null,"abstract":"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.","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

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, Li Tang, Xu Li, Liuye Huang","doi":"10.1002/ccs3.12044","DOIUrl":"10.1002/ccs3.12044","url":null,"abstract":"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.","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, 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","doi":"10.1002/ccs3.12041","DOIUrl":"https://doi.org/10.1002/ccs3.12041","url":null,"abstract":"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 CBR4 promoter region thus downgraded the expression of CBR4, 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 FASN by activating the ubiquitin proteasome pathway and suppressed mTOR signaling. Overall, our results uncovers the CBR4/FASN/mTOR axis as a mechanism for tumor development and inspires us a new molecular guide for the therapeutic strategies for GEP-NETs treatment.","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, Ralf Weiskirchen","doi":"10.1002/ccs3.12039","DOIUrl":"10.1002/ccs3.12039","url":null,"abstract":"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.","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