Open AccessRETRACTED: lnc RNA HOTAIR promotes gastric cancer proliferation and metastasis via targeting miR‐126 to active CXCR 4 and RhoA signaling pathway
Author(s) -
Xiao Jun,
Lai Hao,
Wei ShengHong,
Ye ZaiSheng,
Gong FuSheng,
Chen LuChuan
Publication year - 2019
Publication title -
cancer medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 53
ISSN - 2045-7634
DOI - 10.1002/cam4.1302
Subject(s) - hotair , cancer research , metastasis , gene knockdown , rhoa , cancer , cell growth , biology , cancer cell , long non coding rna , signal transduction , downregulation and upregulation , cell culture , microbiology and biotechnology , biochemistry , genetics , gene
HOTAIR , a well‐known long noncoding RNA s (lnc RNA ), has been recognized to contribute to the tumor metastasis in several tumors. But its role in gastric cancer remains elusive. Here, we reported an increase in HOTAIR promoted proliferation and metastasis of gastric cancer cell lines. The HOTAIR and miR‐126 level was determined in 15 paired primary gastric cancer tissues and their adjacent noncancerous gastric tissues. Over‐expression or downregulation HOTAIR was conducted in AGS or BGC ‐823 cells to investigate the impact of HOTAIR in proliferation and metastasis. Then dual luciferase reporter assay was utilized to study the interaction between CXCR 4 and miR‐126. Cells transfected with sh HOTAIR or miR‐126 mimic were subjected to western blot to investigate the role of SDF ‐1/ CXCR 4 signaling in HOTAIR mediated proliferation and metastasis. HOTAIR was highly expressed in gastric cancer tissues and several gastric cancer cell lines. Overexpressed HOTAIR facilitated proliferation and metastasis in vitro while HOTAIR knockdown inhibit proliferation and metastasis. A negative correlation was observed between miR‐126 and HOTAIR . And, we also confirmed the decrease in miR‐126 in clinic specimen. Furthermore, HOTAIR and miR‐126 negatively regulated each other and then increase or decrease CXCR 4 expression and downstream pathway, respectively. CXCR 4 was confirmed as a direct target of miR‐126. Our study demonstrated that high HOTAIR expression promote proliferation and metastasis in gastric cancer via miR‐126/ CXCR 4 axis and downstream signaling pathways.