MiR-1178 Promotes the Proliferation, G1/S Transition, Migration and Invasion of Pancreatic Cancer Cells by Targeting CHIP

被引:21
|
作者
Cao, Zhe [1 ,2 ]
Xu, Jianwei [1 ,2 ]
Huang, Hua [1 ,2 ]
Shen, Peng [1 ,2 ]
You, Lei [1 ,2 ]
Zhou, Li [1 ,2 ]
Zheng, Lianfang [2 ,3 ]
Zhang, Taiping [1 ,2 ]
Zhao, Yupei [1 ,2 ]
机构
[1] Chinese Acad Med Sci, Peking Union Med Coll Hosp, Dept Gen Surg, Beijing 100730, Peoples R China
[2] Peking Union Med Coll, Beijing 100021, Peoples R China
[3] Chinese Acad Med Sci, Peking Union Med Coll Hosp, Dept Nucl Med, Beijing 100730, Peoples R China
来源
PLOS ONE | 2015年 / 10卷 / 01期
基金
北京市自然科学基金; 中国国家自然科学基金;
关键词
HSC70-INTERACTING PROTEIN; INDUCED DEGRADATION; TUMOR-SUPPRESSOR; C-TERMINUS; MUTANT P53; CARCINOMA; CHAPERONE; GROWTH; ADENOCARCINOMA; INACTIVATION;
D O I
10.1371/journal.pone.0116934
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
CHIP, a co-chaperone protein that interacts with Hsc/Hsp70, has been shown to be underexpressed in pancreatic cancer cells and has demonstrated a potential tumor suppressor property. Nevertheless, the underlying mechanisms of CHIP regulation in pancreatic cancer cells remain unknown. In this study, we found that miR-1178 decreased the translation of the CHIP protein by targeting the 30-UTR region. We observed that over-expression of miR-1178 facilitated the proliferation, G1/S transition, migration and invasion of pancreatic cancer cells. Conversely, the inhibition of miR-1178 expression significantly suppressed these phenotypes. Furthermore, CHIP over-expression abrogated miR-1178-induced cell proliferation and invasion. Our data suggest that miR-1178 acts as an oncomiR in pancreatic cancer cells by inhibiting CHIP expression.
引用
收藏
页数:12
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