Xiu Zhang, Peng Zhang, Xiang Chen, Xianyi Liu, Wenwen Liu, Xi Hu, Chengcheng Sun, Xiaochun Wang, Jianhong Shi
{"title":"去泛素酶 OTUD7B 调控乳腺癌细胞增殖","authors":"Xiu Zhang, Peng Zhang, Xiang Chen, Xianyi Liu, Wenwen Liu, Xi Hu, Chengcheng Sun, Xiaochun Wang, Jianhong Shi","doi":"10.1016/j.clbc.2024.10.002","DOIUrl":null,"url":null,"abstract":"<p><strong>Purpose: </strong>The deubiquitylase OTUD7B plays a facilitates role in lung tumorigenesis through VEGF protein, but its role in breast cancer remains unclear. In the present study, we proposed to explore the role of deubiquitylase OTUD7B in breast cancer.</p><p><strong>Methods: </strong>The expression of OTUD7B in breast cancer and adjacent tissues was detected. The role of OTUD7B in cell proliferation and invasion of breast cancer cell lines such as MCF-7 and MDA-MB-453 was explored.</p><p><strong>Results: </strong>OTUD7B is highly expressed in human breast cancer tissues and its higher expression correlates with better survival of patients. Further mechanistic studies reveal that OTUD7B associates with RASGRF1 and PLCE1 to disrupt RAS signaling pathway. Knockdown of OTUD7B results in decreasing levels of RASGRF1 protein, suppression cell growth and invasion in breast cancer. Collectively, our results reveal a previously unappreciated anti-oncogentic role OTUD7B involved in RAS signaling pathway in breast cancer and indicate that deubiquitylases could induce tumor-suppressing or tumor-promoting activities in a cell- and tissue-dependent context.</p>","PeriodicalId":10197,"journal":{"name":"Clinical breast cancer","volume":" ","pages":""},"PeriodicalIF":2.9000,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Deubiquitinase OTUD7B Regulates Cell Proliferation in Breast Cancer.\",\"authors\":\"Xiu Zhang, Peng Zhang, Xiang Chen, Xianyi Liu, Wenwen Liu, Xi Hu, Chengcheng Sun, Xiaochun Wang, Jianhong Shi\",\"doi\":\"10.1016/j.clbc.2024.10.002\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Purpose: </strong>The deubiquitylase OTUD7B plays a facilitates role in lung tumorigenesis through VEGF protein, but its role in breast cancer remains unclear. In the present study, we proposed to explore the role of deubiquitylase OTUD7B in breast cancer.</p><p><strong>Methods: </strong>The expression of OTUD7B in breast cancer and adjacent tissues was detected. The role of OTUD7B in cell proliferation and invasion of breast cancer cell lines such as MCF-7 and MDA-MB-453 was explored.</p><p><strong>Results: </strong>OTUD7B is highly expressed in human breast cancer tissues and its higher expression correlates with better survival of patients. Further mechanistic studies reveal that OTUD7B associates with RASGRF1 and PLCE1 to disrupt RAS signaling pathway. Knockdown of OTUD7B results in decreasing levels of RASGRF1 protein, suppression cell growth and invasion in breast cancer. Collectively, our results reveal a previously unappreciated anti-oncogentic role OTUD7B involved in RAS signaling pathway in breast cancer and indicate that deubiquitylases could induce tumor-suppressing or tumor-promoting activities in a cell- and tissue-dependent context.</p>\",\"PeriodicalId\":10197,\"journal\":{\"name\":\"Clinical breast cancer\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":2.9000,\"publicationDate\":\"2024-10-22\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Clinical breast cancer\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1016/j.clbc.2024.10.002\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"ONCOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical breast cancer","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1016/j.clbc.2024.10.002","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"ONCOLOGY","Score":null,"Total":0}
Deubiquitinase OTUD7B Regulates Cell Proliferation in Breast Cancer.
Purpose: The deubiquitylase OTUD7B plays a facilitates role in lung tumorigenesis through VEGF protein, but its role in breast cancer remains unclear. In the present study, we proposed to explore the role of deubiquitylase OTUD7B in breast cancer.
Methods: The expression of OTUD7B in breast cancer and adjacent tissues was detected. The role of OTUD7B in cell proliferation and invasion of breast cancer cell lines such as MCF-7 and MDA-MB-453 was explored.
Results: OTUD7B is highly expressed in human breast cancer tissues and its higher expression correlates with better survival of patients. Further mechanistic studies reveal that OTUD7B associates with RASGRF1 and PLCE1 to disrupt RAS signaling pathway. Knockdown of OTUD7B results in decreasing levels of RASGRF1 protein, suppression cell growth and invasion in breast cancer. Collectively, our results reveal a previously unappreciated anti-oncogentic role OTUD7B involved in RAS signaling pathway in breast cancer and indicate that deubiquitylases could induce tumor-suppressing or tumor-promoting activities in a cell- and tissue-dependent context.
期刊介绍:
Clinical Breast Cancer is a peer-reviewed bimonthly journal that publishes original articles describing various aspects of clinical and translational research of breast cancer. Clinical Breast Cancer is devoted to articles on detection, diagnosis, prevention, and treatment of breast cancer. The main emphasis is on recent scientific developments in all areas related to breast cancer. Specific areas of interest include clinical research reports from various therapeutic modalities, cancer genetics, drug sensitivity and resistance, novel imaging, tumor genomics, biomarkers, and chemoprevention strategies.