Journal of Cell Communication and Signaling最新文献

筛选
英文 中文
The 12th international workshop on the CCN family of genes in pictures 第12届CCN家族基因图片国际研讨会。
IF 3.6 3区 生物学
Journal of Cell Communication and Signaling Pub Date : 2024-11-13 DOI: 10.1002/ccs3.12051
Annick Perbal
{"title":"The 12th international workshop on the CCN family of genes in pictures","authors":"Annick Perbal","doi":"10.1002/ccs3.12051","DOIUrl":"10.1002/ccs3.12051","url":null,"abstract":"<p>From June 20th to June 23rd, the 12th International workshop on the CCN Family of Genes has been held at the <b>Scandic Holmenkollen Park Hotel, OSLO–Norway</b></p><p></p><p><b>Organizers</b></p><p>Professor Håvard Attramadal and Dr. Vivi T. Monsen, Oslo University Hospital</p><p><b>Co-organizers</b></p><p>Professor Bernard Perbal and Annick Perbal, International CCN Society, Nice France</p><p>The workshop has been scientifically and socially very successful.</p><p>Since the previous meeting held in Nice in 2022, it has been opened to different fields.</p><p>This year, Dr. Katia Scotlandi from Bologna, Italy, has been selected to be the 9<sup>th</sup> ICCNS Awardee.</p><p></p><p></p><p>Dr. Katia Scotlandi has long been committed to advancing research and scientific interest in the field of IGF and insulin system. Her scientific group has demonstrated the importance of the related signaling pathway in sarcomas, particularly in the Ewing sarcoma and participated in the development of rationale strategies to inhibit IGF1R-mediated signaling at preclinical level. She has also highlighted the role of the insulin receptor in the rapid development of resistance to antibodies targeting IGF1R. More recently, she has introduced the concept that the RNA-binding protein IGF2BP3 may regulate the cell sensitivity to anti-IGF1R agents. In addition she has significantly contributed hard to the identification of novel biomarkers of risk and prognosis, including CCN3, as well as of new therapeutic targets for these tumors. More recently, she has developed a platform for sequencing and establishment of complex preclinical models to accelerate our understanding of bone sarcomas.</p><p></p><p><b>Listing of the ICCNS awardees</b></p><p><b>Program</b></p><p><b>T</b><b>hursday, June 20</b></p><p><b>9:00 Registration begins</b></p><p><b>10:30–11:30 Business meeting for the JCCS Editorial Board.</b></p><p><b>11:45–13:00 Lunch</b></p><p><b>Workshop Opening</b></p><p></p><p></p><p><b>Session I</b></p><p><b>ECM Proteins in Cell Communication and Signaling</b></p><p><b>Chairs: Brahim Chaqour and Vivi T. Monsen</b></p><p></p><p></p><p><b>14:40–15:10 Coffee Break</b></p><p></p><p></p><p></p><p><b>18:30 Welcome reception and Dinner with Live Music at Scandic Holmenkollen Park Hotel</b></p><p><b>Session II</b></p><p><b>Vascular Development and Pathophysiology</b></p><p><b>Chairs: Lester Lau and Håvard Attramadal</b></p><p></p><p></p><p></p><p><b>9:50–10:20 Coffee Break</b></p><p></p><p></p><p></p><p><b>Session III</b></p><p><b>Mechanisms of Diseases: Fibrosis and The Matrix</b></p><p><b>Chairs: George Bou-Gharios and Satoshi Kubota</b></p><p></p><p></p><p><b>Lunch 12:10–13:30</b></p><p></p><p></p><p></p><p></p><p></p><p><b>Boat Trip on the Oslo Fjord with dinner</b></p><p></p><p><b>Saturday, June 22</b></p><p><b>Session IV</b></p><p><b>Tissue Development and Homeostasis</b></p><p><b>Chairs: Blandine Poulet and Bernard Perbal</b></p><p></p><p></p><p></p><p><b>9:45–10:15 Coffee ","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"18 4","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11647047/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142846774","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
Emerging role of IRE1α in vascular diseases IRE1α在血管疾病中的新作用。
IF 3.6 3区 生物学
Journal of Cell Communication and Signaling Pub Date : 2024-11-10 DOI: 10.1002/ccs3.12056
Jia Shi, Fan He, Xiaogang Du
{"title":"Emerging role of IRE1α in vascular diseases","authors":"Jia Shi,&nbsp;Fan He,&nbsp;Xiaogang Du","doi":"10.1002/ccs3.12056","DOIUrl":"10.1002/ccs3.12056","url":null,"abstract":"<p>A mounting body of evidence suggests that the endoplasmic reticulum stress and the unfolded protein response are involved in the underlying mechanisms responsible for vascular diseases. Inositol-requiring protein 1α (IRE1α), the most ancient branch among the UPR-related signaling pathways, can possess both serine/threonine kinase and endoribonuclease (RNase) activity and can perform physiological and pathological functions. The IRE1α-signaling pathway plays a critical role in the pathology of various vascular diseases. In this review, we provide a general overview of the physiological function of IRE1α and its pathophysiological role in vascular diseases.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"18 4","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11647051/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142846699","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
Exploring the dual role of endoplasmic reticulum stress in urological cancers: Implications for tumor progression and cell death interactions 探索内质网应激在泌尿系统癌症中的双重作用:对肿瘤进展和细胞死亡相互作用的影响。
IF 3.6 3区 生物学
Journal of Cell Communication and Signaling Pub Date : 2024-11-03 DOI: 10.1002/ccs3.12054
Najma Farahani, Mina Alimohammadi, Mehdi Raei, Noushin Nabavi, Amir Reza Aref, Kiavash Hushmandi, Salman Daneshi, Alireza Razzaghi, Afshin Taheriazam, Mehrdad Hashemi
{"title":"Exploring the dual role of endoplasmic reticulum stress in urological cancers: Implications for tumor progression and cell death interactions","authors":"Najma Farahani,&nbsp;Mina Alimohammadi,&nbsp;Mehdi Raei,&nbsp;Noushin Nabavi,&nbsp;Amir Reza Aref,&nbsp;Kiavash Hushmandi,&nbsp;Salman Daneshi,&nbsp;Alireza Razzaghi,&nbsp;Afshin Taheriazam,&nbsp;Mehrdad Hashemi","doi":"10.1002/ccs3.12054","DOIUrl":"10.1002/ccs3.12054","url":null,"abstract":"<p>The endoplasmic reticulum (ER) is crucial for maintaining calcium balance, lipid biosynthesis, and protein folding. Disruptions in ER homeostasis, often due to the accumulation of misfolded or unfolded proteins, lead to ER stress, which plays a significant role in various diseases, especially cancer. Urological cancers, which account for high male mortality worldwide, pose a persistent challenge due to their incurability and tendency to develop drug resistance. Among the numerous dysregulated biological mechanisms, ER stress is a key factor in the progression and treatment response of these cancers. This review highlights the dual role of aberrant ER stress activation in urologic cancers, affecting both tumor growth and therapeutic outcomes. While ER stress can support tumor growth through pro-survival autophagy, it primarily inhibits cancer progression via apoptosis and pro-death autophagy. Interestingly, ER stress can paradoxically aid cancer progression through mechanisms such as exosome-mediated immune evasion. Additionally, the review examines how pharmacological interventions, particularly with phytochemicals, can stimulate ER stress-mediated tumor suppression. Key regulators, including PERK, IRE1α, and ATF6, are discussed for their roles in upregulating CHOP levels and triggering apoptosis. In conclusion, a deeper understanding of ER stress in urological cancers not only clarifies the complex interactions between cellular stress and cancer progression but also provides new opportunities for innovative therapeutic strategies.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"18 4","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11647052/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142846706","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
Correction to “LncRNA HOTTIP promotes LPS-induced lung epithelial cell injury by recruiting DNMT1 to epigenetically regulate SP-C” 更正“LncRNA HOTTIP通过招募DNMT1通过表观遗传调控SP-C促进lps诱导的肺上皮细胞损伤”。
IF 3.6 3区 生物学
Journal of Cell Communication and Signaling Pub Date : 2024-10-31 DOI: 10.1002/ccs3.12042
{"title":"Correction to “LncRNA HOTTIP promotes LPS-induced lung epithelial cell injury by recruiting DNMT1 to epigenetically regulate SP-C”","authors":"","doi":"10.1002/ccs3.12042","DOIUrl":"10.1002/ccs3.12042","url":null,"abstract":"<p>Li, S., Li, S., Gao, Z. and Liu, Y. (2024), LncRNA HOTTIP promotes LPS-induced lung epithelial cell injury by recruiting DNMT1 to epigenetically regulate SP-C. <i>J. Cell Commun. Signal</i>, 18: e12020. https://doi.org/10.1002/ccs3.12020.</p><p>In the originally published article, the funding number was omitted. The correct sentence is:</p><p>The research was sponsored by the Scientific Research Project of Heilongjiang Health Commission (No. 2020-332).</p><p>We apologize for this error.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"18 4","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11647046/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142846690","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
Role for the PIP2-binding protein myristoylated alanine-rich C-kinase substrate in vascular tissue: A novel therapeutic target for cardiovascular disease pip2结合蛋白肉豆蔻酰基化富丙氨酸c激酶底物在血管组织中的作用:心血管疾病的新治疗靶点
IF 3.6 3区 生物学
Journal of Cell Communication and Signaling Pub Date : 2024-10-02 DOI: 10.1002/ccs3.12052
Anthony P. Albert, Kazi S. Jahan, Harry Z. E. Greenberg, Yousif A. Shamsaldeen
{"title":"Role for the PIP2-binding protein myristoylated alanine-rich C-kinase substrate in vascular tissue: A novel therapeutic target for cardiovascular disease","authors":"Anthony P. Albert,&nbsp;Kazi S. Jahan,&nbsp;Harry Z. E. Greenberg,&nbsp;Yousif A. Shamsaldeen","doi":"10.1002/ccs3.12052","DOIUrl":"10.1002/ccs3.12052","url":null,"abstract":"<p>In vascular smooth muscle cells (VSMCs) and vascular endothelial cells (VECs), phosphatidylinositol 4,5-bisphosphate (PIP<sub>2</sub>) acts as a substrate for phospholipase C (PLC)- and phosphoinositol 3-kinase (PI3K)-mediated signaling pathways and an unmodified ligand at ion channels and other macromolecules, which are key processes in the regulation of cell physiological and pathological phenotypes. It is envisaged that these distinct roles of PIP<sub>2</sub> are achieved by PIP<sub>2</sub>-binding proteins, which act as PIP<sub>2</sub> buffers to produce discrete pools of PIP<sub>2</sub> that permits targeted release within the cell. This review discusses evidence for the expression, cell distribution, and role of myristoylated alanine-rich C-kinase substrate (MARCKS), a PIP<sub>2</sub>-binding protein, in cellular signaling and function of VSMCs. The review indicates the possibilities for MARCKS as a therapeutic target for vascular disease involving dysfunctional cell proliferation and migration, endothelial barrier permeability, and vascular contractility such as atherosclerosis, systemic and pulmonary hypertension, and sepsis.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"18 4","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11647048/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142846739","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
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,&nbsp;Qian Liu,&nbsp;Shen Wu,&nbsp;Xiaowei Fan,&nbsp;Yufei Teng,&nbsp;Ningli Wang,&nbsp;Jingxue Zhang","doi":"10.1002/ccs3.12050","DOIUrl":"https://doi.org/10.1002/ccs3.12050","url":null,"abstract":"<p>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.</p>","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
{"title":"Association for research on biosignaling and communication first world conference on cellular communication and signaling","authors":"Bernard Perbal,&nbsp;Ralf Weiskirchen","doi":"10.1002/ccs3.12048","DOIUrl":"https://doi.org/10.1002/ccs3.12048","url":null,"abstract":"<p>The present manuscript reports on the progress made toward the official announcement of the first World Conference on Cellular Communication and Signaling. This conference is made possible by the Association for research on biosignaling and communication initiative, which was originally launched in 2020 and revitalized during the 12th International Workshop on the Cell Communication Network family of genes in Oslo (June 20–23, 2024). The aim of this conference is to facilitate interactions among the members of societies interested in all aspects of research on Biosignaling and Communication. It is intended to provide a platform for collaborative efforts aimed at unraveling and understanding the functioning of biological pathways in both normal and pathological conditions.</p>","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/ccs3.12048","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142275072","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
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,&nbsp;Ralf Weiskirchen,&nbsp;Bernard Perbal","doi":"10.1002/ccs3.12049","DOIUrl":"https://doi.org/10.1002/ccs3.12049","url":null,"abstract":"<p>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.</p>","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,&nbsp;Maria Antonella Laginestra,&nbsp;Maria Cristina Manara,&nbsp;Lorena Landuzzi,&nbsp;Francesca Ruzzi,&nbsp;Margherita Maioli,&nbsp;Evelin Pellegrini,&nbsp;Alessandra De Feo,&nbsp;Pier-Luigi Lollini,&nbsp;Katia Scotlandi","doi":"10.1002/ccs3.12047","DOIUrl":"https://doi.org/10.1002/ccs3.12047","url":null,"abstract":"<p>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.</p>","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,&nbsp;Chi-Hou Ng,&nbsp;Yu-Fu Chen,&nbsp;Yu-Chun Wang,&nbsp;I-Shing Yu,&nbsp;Lukas Jyuhn-Hsiarn Lee,&nbsp;Li-Jen Lee,&nbsp;Kuang-Yung Lee","doi":"10.1002/ccs3.12040","DOIUrl":"10.1002/ccs3.12040","url":null,"abstract":"<p>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 <i>Ccn2</i> knockout (Fb<i>Ccn2</i> KO) mice. In this study, we examined the behavioral phenotypes of Fb<i>Ccn2</i>KO 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 Fb<i>Ccn2</i><sup>−/−</sup> mice as compared to controls. However, in the prefrontal cortex, RIT-induced c-fos levels in Fb<i>Ccn2</i><sup>−/−</sup> 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.</p>","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
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
相关产品
×
本文献相关产品
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信