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KCNQ1OT1 facilitates progression of non‐small‐cell lung carcinoma via modulating miRNA‐27b‐3p/HSP90AA1 axis
Author(s) -
Dong Zhiwu,
Yang Ping,
Qiu Xiaojian,
Liang Shuang,
Guan Bing,
Yang Haisheng,
Li Feifei,
Sun Li,
Liu Huiling,
Zou Guanghui,
Zhao Kewen
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.27788
Subject(s) - gene knockdown , carcinogenesis , microrna , cancer research , oncogene , lung cancer , cell growth , long non coding rna , tumor progression , cell , metastasis , biology , downregulation and upregulation , cancer , medicine , cell culture , oncology , gene , cell cycle , genetics
Long noncoding RNA KCNQ1OT1 participates in the regulation of imprinted genes within the kcnq1 domain. But its roles in carcinogenesis and metastasis remain largely elusive. Herein, we evaluated its potential in non‐small‐cell lung cancer (NSCLC) progression. We demonstrated that the KCNQ1OT1 level was upregulated in NSCLC tissues and cell lines. High KCNQ1OT1 level correlated with poor overall and progression‐free survival in NSCLC patients. KCNQ1OT1 facilitated proliferation, migration, and invasion in H460 cells. Furthermore, knockdown of KCNQ1OT1 reduced the expression of HSP90AA1. KCNQ1OT1 presented a positive correlation with HSP90AA1 which predicted the tumor progression in NSCLC from The Cancer Genome Atlas database. Intriguingly, KCNQ1OT1 modulated HSP90AA1 expression by sponging miR‐27b‐3p. MiR‐27b‐3p counteracted the effect of KCNQ1OT1 on HSP90AA1 expression, H460 cell migration, and invasion. These data revealed a role for KCNQ1OT1 as an oncogene through miR‐27b‐3p/HSP90AA1 axis during NSCLC progression.