Open AccessUCA 1 promotes cell proliferation and invasion of gastric cancer by targeting CREB 1 sponging to miR‐590‐3p
Author(s) -
Gu Lei,
Lu Liesheng,
Zhou Donglei,
Liu Zhongchen
Publication year - 2018
Publication title -
cancer medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 53
ISSN - 2045-7634
DOI - 10.1002/cam4.1310
Subject(s) - gene knockdown , oncogene , cell growth , biology , carcinogenesis , cancer research , downregulation and upregulation , long non coding rna , cancer , cell , creb , microbiology and biotechnology , cell culture , cell cycle , gene , transcription factor , biochemistry , genetics
Long noncoding RNA s (lnc RNA s) have emerged as regulators in a variety of biological processes, including carcinogenesis in human cancer. UCA 1 has been reported to be upregulated in gastric cancer ( GC ); however, the underlying functional roles of UCA 1 in GC have not been established. In the current study, we showed that UCA 1 is significantly higher in GC tissues and cells compared with adjacent normal tissues and a gastric epithelium cell line, respectively. Higher UCA 1 expression was associated with lymph node metastasis, TNM stage, and poor overall survival ( OS ) in GC patients. In vitro functional studies confirmed that UCA 1 promotes cell proliferation, colony formation ability, and cell invasion in GC cells. We demonstrated that knockdown of UCA 1 inhibits tumor growth in vivo. The double luciferase reporter, RNA‐binding protein immunoprecipitation assay, and RNA pull down assay demonstrated that miR‐590‐3p serves as a target for UCA 1. UCA 1 promoted cell proliferation and invasion by negatively regulating miR‐590‐3p expression. Moreover, we demonstrated that CREB 1 is a downstream target of miR‐590‐3p and UCA 1 activates CREB 1 expression by sponging to miR‐590‐3p. Thus, these results showed that UCA 1 functions as an oncogene in GC and may be a target for treatment of GC .