Open AccessmiR‑512‑5p suppresses the progression of non‑small cell lung cancer by targeting β‑catenin
Author(s) -
Zhexin Wang,
Xiaolei Zhu,
Tuo Zhang,
Feng Yao
Publication year - 2019
Publication title -
oncology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.766
H-Index - 54
eISSN - 1792-1082
pISSN - 1792-1074
DOI - 10.3892/ol.2019.11102
Subject(s) - oncogene , molecular medicine , cell cycle , cell cycle progression , cancer research , cancer , lung cancer , catenin , cell , apoptosis , biology , medicine , oncology , wnt signaling pathway , microbiology and biotechnology , genetics , signal transduction
The oncogenic protein β-catenin is regulated by microRNAs (miRs) in non-small cell lung cancer (NSCLC). miR-512-5p is downregulated in NSCLC compared with healthy tissues and exhibits a tumour-suppressive effect. To study whether miR-512-5p acts on β-catenin to exert its anticancer effect in NSCLC, miR-512-5p mimic and inhibitor were transfected into NSCLC A549 and H1975 cells. miR-512-5p mimic inhibited the invasion of NSCLC cells and increased apoptosis, which suggested an inhibitory effect of miR-512-5p in NSCLC progression in vitro . By contrast, transfection with the miR-512-5p inhibitor resulted in the opposite effects. A dual-luciferase assay demonstrated that miR-512-5p complementarily bound to the 3'-untranslated region of β-catenin. miR-512-5p mimic suppressed the transcription and translation of β-catenin and reduced the expression of the downstream oncogenes cyclin D1 and matrix metalloproteinases, leading to the inhibition of Wnt/β-catenin signalling and subsequent inhibition of NSCLC tumourigenesis in vitro . In conclusion, miR-512-5p may function as a tumour suppressor in NSCLC by inhibiting the Wnt/β-catenin pathway.