Eur Rev Med Pharmacol Sci 2019; 23 (8): 3383-3389

DOI: 10.26355/eurrev_201904_17702

Long noncoding RNA MIAT promotes the growth and metastasis of non-small cell lung cancer by upregulating TDP43

H.-L. Zhao, S.-Q. Xu, Q. Li, Y.-B. Zhao, X. Li, M.-P. Yang

Department of Medicine, Harbin Medical University Cancer Hospital, Harbin, China. yangmaopeng1@163.com


OBJECTIVE: Recent researches have proved that long noncoding RNAs (lncRNAs) act and have an important role in many diseases. In this research, lncRNA MIAT was explored to identify how it functions in the development of non-small cell lung cancer (NSCLC).
PATIENTS AND METHODS: Real-time quantitative polymerase chain reaction (RT-qPCR) was utilized to detect MIAT expression in NSCLC patients. Next, we conducted cell counting kit-8 (CCK-8) assay, colony formation assay, ethynyl deoxyuridine (EdU) incorporation assay, wound healing assay and transwell assay to identify its biological function. Further experiments were performed to explore the potential mechanism.
RESULTS: By comparing with MIAT expression in adjacent tissues, MIAT expression level was significantly higher in NSCLC samples. Moreover, functional assays showed that cell growth ability of NSCLC cells was inhibited after MIAT was knocked down. In addition, the migrated and invaded ability of NSCLC cells was inhibited after MIAT was knocked down. Furthermore, the expression of TDP43 was downregulated by knockdown of MIAT. Meanwhile, it was found that TDP43 expression positively correlated to MIAT expression in NSCLC tissues.
CONCLUSIONS: Results above suggest that MIAT could enhance cell proliferation and metastasis of NSCLC by upregulating TDP43, which suggests that MIAT may be a potential therapeutic target in NSCLC.

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To cite this article

H.-L. Zhao, S.-Q. Xu, Q. Li, Y.-B. Zhao, X. Li, M.-P. Yang
Long noncoding RNA MIAT promotes the growth and metastasis of non-small cell lung cancer by upregulating TDP43

Eur Rev Med Pharmacol Sci
Year: 2019
Vol. 23 - N. 8
Pages: 3383-3389
DOI: 10.26355/eurrev_201904_17702