Yulin Guo, Feng Cao, Shun Hu, Shuang Liu, Haichen Sun, Ang Li, Fei Li
{"title":"TMEM176A通过抑制ERK信号传导在胰腺癌中发挥抑癌基因的作用。","authors":"Yulin Guo, Feng Cao, Shun Hu, Shuang Liu, Haichen Sun, Ang Li, Fei Li","doi":"","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Pancreatic cancer is the 7th leading cause of cancer-related death worldwide. Aberrant expressions of transmembrane 176A (TMEM176A) were found in multiple cancer types. However, the expression and function of TMEM176A remain unclear in pancreatic cancer.</p><p><strong>Materials and methods: </strong>Immunohistochemistry, flow cytometry, western blot, and transwell were applied on investigating samples from pancreatic cancer patients and pancreatic cancer cell lines.</p><p><strong>Results: </strong>Analysis based on the TCGA database showed that a high level of TMEM176A was associated with a better relapse-free survival rate (P = 0.012). Further, the results of tissue microarray showed patients with a high level of TMEM176A were associated with lymph node metastasis (P = 0.045) and a better overall survival rate (P = 0.032). Overexpression of TMEM176A in Capan-1 and PANC-1 cells suppressed cell proliferation, cell invasion, and migration, and induced apoptosis in pancreatic cancer cells. TMEM176A suppressed ERK signaling in pancreatic cancer.</p><p><strong>Conclusion: </strong>TMEM176A suppresses the growth and migration of pancreatic cancer cells by inhibiting ERK signaling.</p>","PeriodicalId":11379,"journal":{"name":"Discovery medicine","volume":"30 161","pages":"145-153"},"PeriodicalIF":2.0000,"publicationDate":"2020-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"TMEM176A acts as a tumor suppressor gene in pancreatic cancer by inhibiting ERK signaling.\",\"authors\":\"Yulin Guo, Feng Cao, Shun Hu, Shuang Liu, Haichen Sun, Ang Li, Fei Li\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Pancreatic cancer is the 7th leading cause of cancer-related death worldwide. Aberrant expressions of transmembrane 176A (TMEM176A) were found in multiple cancer types. However, the expression and function of TMEM176A remain unclear in pancreatic cancer.</p><p><strong>Materials and methods: </strong>Immunohistochemistry, flow cytometry, western blot, and transwell were applied on investigating samples from pancreatic cancer patients and pancreatic cancer cell lines.</p><p><strong>Results: </strong>Analysis based on the TCGA database showed that a high level of TMEM176A was associated with a better relapse-free survival rate (P = 0.012). Further, the results of tissue microarray showed patients with a high level of TMEM176A were associated with lymph node metastasis (P = 0.045) and a better overall survival rate (P = 0.032). Overexpression of TMEM176A in Capan-1 and PANC-1 cells suppressed cell proliferation, cell invasion, and migration, and induced apoptosis in pancreatic cancer cells. TMEM176A suppressed ERK signaling in pancreatic cancer.</p><p><strong>Conclusion: </strong>TMEM176A suppresses the growth and migration of pancreatic cancer cells by inhibiting ERK signaling.</p>\",\"PeriodicalId\":11379,\"journal\":{\"name\":\"Discovery medicine\",\"volume\":\"30 161\",\"pages\":\"145-153\"},\"PeriodicalIF\":2.0000,\"publicationDate\":\"2020-11-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Discovery medicine\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"MEDICINE, RESEARCH & EXPERIMENTAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Discovery medicine","FirstCategoryId":"3","ListUrlMain":"","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
TMEM176A acts as a tumor suppressor gene in pancreatic cancer by inhibiting ERK signaling.
Background: Pancreatic cancer is the 7th leading cause of cancer-related death worldwide. Aberrant expressions of transmembrane 176A (TMEM176A) were found in multiple cancer types. However, the expression and function of TMEM176A remain unclear in pancreatic cancer.
Materials and methods: Immunohistochemistry, flow cytometry, western blot, and transwell were applied on investigating samples from pancreatic cancer patients and pancreatic cancer cell lines.
Results: Analysis based on the TCGA database showed that a high level of TMEM176A was associated with a better relapse-free survival rate (P = 0.012). Further, the results of tissue microarray showed patients with a high level of TMEM176A were associated with lymph node metastasis (P = 0.045) and a better overall survival rate (P = 0.032). Overexpression of TMEM176A in Capan-1 and PANC-1 cells suppressed cell proliferation, cell invasion, and migration, and induced apoptosis in pancreatic cancer cells. TMEM176A suppressed ERK signaling in pancreatic cancer.
Conclusion: TMEM176A suppresses the growth and migration of pancreatic cancer cells by inhibiting ERK signaling.
期刊介绍：
Discovery Medicine publishes novel, provocative ideas and research findings that challenge conventional notions about disease mechanisms, diagnosis, treatment, or any of the life sciences subjects. It publishes cutting-edge, reliable, and authoritative information in all branches of life sciences but primarily in the following areas: Novel therapies and diagnostics (approved or experimental); innovative ideas, research technologies, and translational research that will give rise to the next generation of new drugs and therapies; breakthrough understanding of mechanism of disease, biology, and physiology; and commercialization of biomedical discoveries pertaining to the development of new drugs, therapies, medical devices, and research technology.
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