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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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Cite This Article

APA Style
Ma, Y., Feng, J., Xing, X., Zhou, B., Li, S. et al. (2016). Mir-1908 overexpression inhibits proliferation, changing akt activity and p53 expression in hypoxic NSCLC cells. Oncology Research, 24(1), 9-15. https://doi.org/10.3727/096504016X14570992647168
Vancouver Style
Ma Y, Feng J, Xing X, Zhou B, Li S, Zhang W, et al. Mir-1908 overexpression inhibits proliferation, changing akt activity and p53 expression in hypoxic NSCLC cells. Oncol Res. 2016;24(1):9-15 https://doi.org/10.3727/096504016X14570992647168
IEEE Style
Y. Ma et al., “miR-1908 Overexpression Inhibits Proliferation, Changing Akt Activity and p53 Expression in Hypoxic NSCLC Cells,” Oncol. Res., vol. 24, no. 1, pp. 9-15, 2016. https://doi.org/10.3727/096504016X14570992647168



cc Copyright © 2016 The Author(s). Published by Tech Science Press.
This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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