Open AccessmiR‐1 suppresses the proliferation and promotes the apoptosis of esophageal carcinoma cells by targeting Src
Author(s) -
Liao Zhicong,
Wang Xiaojun,
Liang Hongwei,
Yu Ao,
ur Rehman Uzair,
Fan Qian,
Hu Yue,
Wang Chen,
Zhou Zhen,
Wang Tao
Publication year - 2017
Publication title -
cancer medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 53
ISSN - 2045-7634
DOI - 10.1002/cam4.1214
Subject(s) - proto oncogene tyrosine protein kinase src , gene knockdown , cancer research , esophageal cancer , oncogene , microrna , apoptosis , tyrosine kinase , suppressor , biology , cell growth , microbiology and biotechnology , mechanism (biology) , cancer , signal transduction , cell cycle , gene , genetics , philosophy , epistemology
Nonreceptor tyrosine kinase c‐Src, also known as Src, is a potent oncogene involved in a series of biological processes including cell growth, differentiation, and apoptosis; however, its expression pattern and function in esophageal cancer is poorly addressed. In this study, abnormal overexpression of Src protein was observed in esophageal cancer tissues, which fuelled the speculation that microRNA‐mediated posttranscriptional regulatory mechanism might be involved. Bioinformatic analyses were applied to identify miRNAs that could potentially target Src. miR‐1 was predicted and further validated as a direct repressor of Src. Moreover, we manipulated knockdown and overexpression experiment on TE‐1 and TE‐10 cells to demonstrate miR‐1 suppressed proliferation and promoted apoptosis in esophageal cancer cells by inhibiting Src. Taken together, this study underlines a negative regulatory mechanism in which miR‐1 serves as a suppressor of Src in esophageal cancer cells and may provide insights into novel therapeutic approaches for esophageal cancer.