Open Access

ARTICLE

miR-1908 Overexpression Inhibits Proliferation, Changing Akt Activity and p53 Expression in Hypoxic NSCLC Cells

Yuefeng Ma^*, Jie Feng^†, Xin Xing^‡, Bin Zhou^*, Shaomin Li^*, Wei Zhang^*, Jiantao Jiang^*, Jin Zhang^*, Zhe Qiao^*, Liangzhang Sun^*, Zhenchuan Ma^*, Ranran Kong^*

* Department of Thoracic Surgery, the Second Affiliated Hospital of Medical School, Xi’an Jiaotong University, Xi’an, Shaanxi, China
† Department of Nephrology, the First Affiliated Hospital of Medical School, Xi’an Jiaotong University, Xi’an, Shaanxi, China
‡ Department of Health Care for Cadres, the Second Affiliated Hospital of Medical School, Xi’an Jiaotong University, Xi’an, Shaanxi, China

Oncology Research 2016, 24(1), 9-15. https://doi.org/10.3727/096504016X14570992647168

Abstract

The ribosomal protein (RP)–p53 pathway has been shown to play a key role in apoptosis and senescence of cancer cells. miR-1908 is a newly found miRNA that was reported to have prognostic potential in melanoma. However, its role and mechanism in the progression of non-small cell lung cancer (NSCLC) are largely unknown. In this study, we found that expression of miR-1908 was significantly downregulated in human NSCLC cell lines, including SK-MES-1, A549, and NCI-H460. Then the role of miR-1908 in NSCLC cell proliferation was explored. The miR-1908 mimic was transfected into NSCLC cell lines, and their proliferation was detected. MTT and Cell Titer-Blue H analyses showed that the cell proliferation was notably reduced by the miR-1908 mimic transfection. Moreover, we found the RP–p53 pathway was activated by miR-1908 mimic. Moreover, the miR-1908 inhibitor transfection had a completely opposite effect on the NSCLC cell proliferation than that of miR-1908 mimic. To explore the underlying mechanism of that, TargetScan bioinformatics server and 3'-UTR luciferase reporter assay were applied to identify the targets of miR-1908. Our results showed that AKT1 substrate 1 (AKT1S1), a newly proven suppressor of the RP–p53 pathway, was a target of miR-1908, suggesting a probable mechanism for miR-191 suppressing NSCLC cell proliferation. Our findings provide a novel molecular target for the regulation of NSCLC cell proliferation.

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Keywords

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