Open AccessmiR‑3120‑5p acts as a diagnostic biomarker in non‑small cell lung cancer and promotes cancer cell proliferation and invasion by targeting KLF4
Author(s) -
Hongwei Xu,
Quan Wen
Publication year - 2018
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2018.9454
Subject(s) - klf4 , cell cycle , cancer research , downregulation and upregulation , cancer , lung cancer , oncogene , metastasis , cell growth , cell , biology , microrna , cancer cell , medicine , sox2 , transcription factor , biochemistry , genetics , gene
Accumulating evidence indicates that microRNAs (miRs) are important regulators in a number of types of human cancer, including non‑small cell lung cancer (NSCLC). The function of miR‑3120‑5p in NSCLC remains unclear. In the present study, it was demonstrated that miR‑3120‑5p was significantly upregulated in NSCLC tissues. Additionally, miR‑3120‑5p expression level was positively associated with NSCLC metastasis and tumor, node and metastasis stage. Furthermore, it was demonstrated that miR‑3120‑5p exhibited potential as an indicator of NSCLC for use in diagnosis. Through functional experiments, it was demonstrated that overexpression of miR‑3120‑5p promoted the proliferation, colony formation and invasion of NSCLC cells. miR‑3120‑5p overexpression significantly promoted cell cycle progression. Mechanistically, it was demonstrated that Krueppel‑like factor 4 (KLF4) was a target of miR‑3120‑5p in NSCLC cells. Overexpression of miR‑3120‑5p repressed the expression of KLF4 in A549 and H460 cells. Furthermore, it was demonstrated that KLF4 was downregulated in NSCLC tissues and cell lines. Overexpression of KLF4 significantly reversed the effects of miR‑3120‑5p on NSCLC cell proliferation and invasion. In conclusion, the present study demonstrated that miR‑3120‑5p promoted NSCLC progression by directly targeting KLF4.