TMEM176A acts as a tumor suppressor gene in pancreatic cancer by inhibiting ERK signaling.

IF 2 4区医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL

Discovery medicine Pub Date : 2020-11-01

Yulin Guo, Feng Cao, Shun Hu, Shuang Liu, Haichen Sun, Ang Li, Fei Li

{"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":"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.","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}

引用次数: 0

Abstract

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.

本刊更多论文

TMEM176A通过抑制ERK信号传导在胰腺癌中发挥抑癌基因的作用。

背景:胰腺癌是全球癌症相关死亡的第七大原因。跨膜蛋白176A (TMEM176A)在多种癌症类型中均有异常表达。然而，TMEM176A在胰腺癌中的表达和功能尚不清楚。材料与方法:采用免疫组织化学、流式细胞术、western blot、transwell等方法对胰腺癌患者及胰腺癌细胞系样本进行研究。结果:基于TCGA数据库的分析显示，高水平的TMEM176A与较高的无复发生存率相关(P = 0.012)。此外，组织芯片结果显示，TMEM176A水平高的患者与淋巴结转移相关(P = 0.045)，总生存率更高(P = 0.032)。胰腺癌Capan-1和PANC-1细胞中过表达TMEM176A可抑制细胞增殖、侵袭和迁移，诱导细胞凋亡。TMEM176A抑制胰腺癌中的ERK信号。结论:TMEM176A通过抑制ERK信号传导抑制胰腺癌细胞的生长和迁移。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Discovery medicine MEDICINE, RESEARCH & EXPERIMENTAL-

CiteScore

5.40

自引率

0.00%

发文量

审稿时长

6-12 weeks

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.