Knockdown of lncRNA MIAT inhibits proliferation and cisplatin resistance in non‑small cell lung cancer cells by increasing miR‑184 expression

Wu,Longqiu; Liu,Chi; Zhang,Zuxiong

doi:10.3892/ol.2019.11084

Knockdown of lncRNA MIAT inhibits proliferation and cisplatin resistance in non‑small cell lung cancer cells by increasing miR‑184 expression

Authors:
- Longqiu Wu
- Chi Liu
- Zuxiong Zhang
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Affiliations: Department of Cardiothoracic Surgery, First Affiliated Hospital of Gannan Medical University, Ganzhou, Jiangxi 341000, P.R. China, School of Medical and Life Sciences, Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan 610072, P.R. China
Published online on: November 13, 2019 https://doi.org/10.3892/ol.2019.11084
Pages: 533-541

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Abstract

Accumulating evidence has demonstrated the important role of long non‑coding RNA myocardial infarction‑associated transcript (MIAT) in tumorigenesis as a potential oncogene. However, the function of MIAT in non‑small cell lung cancer (NSCLC) has yet to be completely elucidated. The present study demonstrated that MIAT expression was significantly upregulated in NSCLC tissues, particularly in aggressive cases, and was highly associated with a poor prognosis. In addition, the upregulated expression of MIAT was observed in cisplatin (CDDP)‑resistant H1299 cells. Knockdown of MIAT inhibited the proliferation of NSCLC cells and enhanced the sensitivity of NSCLC cells to CDDP in vitro and in vivo. Further functional analysis demonstrated that MIAT partially exerted its oncogenic effect by upregulating the expression of splicing factor 1 (SF1), by serving as a microRNA (miR)‑184 sponge. In conclusion, the present study identified that MIAT functions as a competitive endogenous RNA of miR‑184to modulate SF1 expression in NSCLC, which provides a novel insight into the potential therapeutic application of MIAT in NSCLC progression.

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