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.
Keywords: cisplatin resistance; miR-184; myocardial infarction-associated transcript; non-small cell lung cancer; splicing factor 1.
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