Open AccessmiR‐15b enhances the proliferation and migration of lung adenocarcinoma by targeting BCL2
Author(s) -
Wang Jun,
Yao Shupeng,
Diao Yanping,
Geng Yan,
Bi Yanling,
Liu Guangyue
Publication year - 2020
Publication title -
thoracic cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.823
H-Index - 28
eISSN - 1759-7714
pISSN - 1759-7706
DOI - 10.1111/1759-7714.13382
Subject(s) - microrna , cancer research , adenocarcinoma , medicine , cell migration , cell growth , viability assay , lung cancer , cell , cancer , oncology , biology , gene , genetics
Background Lung adenocarcinoma (LUAD) is a subtype of lung cancer (LC), which is the most common tumor worldwide. Accumulating evidence has elucidated an important role of microRNAs (miRNAs) in mediating the development and progression of several tumors. The purpose of this study was to explore the role and underlying mechanism of miR‐15b in LUAD. Methods CCK‐8 and Transwell assays were conducted to measure the capacities of cell viability and migration in SPC‐A1 cells. Luciferase assay was utilized to verifymiR‐15b direct binding to BCL2 mRNA 3′‐UTR. Results We determined that miR‐15b was overexpressed in LUAD and miR‐15b overexpression predicted a significantly worse outcome in patients with LUAD. miR‐15b improved LUAD growth in vitro and vivo. miR‐15b enhanced cell migration and epithelial–mesenchymal transition (EMT) in LUAD. miR‐15b promoted cell viability, migration and EMT through inhibiting BCL2 expression by targeting to its mRNA 3′‐UTR. BCL2 reversed functions of miR‐15b on promoting cell proliferation, migration and EMT in SPC‐A1 cells. Conclusions miR‐15b promoted cell viability, migration and EMT by targeting BCL2 in LUAD. The newly identified miR‐15b/BCL2 axis provides a novel insight into the pathogenesis of LUAD.