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

被引：22

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：

中国国家自然科学基金; 北京市自然科学基金;

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

页数：12

共 39 条

[1]

[Anonymous], 2010, CANCER RES, DOI DOI 10.1158/1538-7445.AM10-5703

[2]

Ballinger CA, 1999, MOL CELL BIOL, V19, P4535

[3] MicroRNAs: Target Recognition and Regulatory Functions [J].