Abstract
Long noncoding RNAs (lncRNAs) play crucial roles in carcinogenesis. Myocardial infarction-associated transcript (MIAT), originally isolated as a candidate gene for myocardial infarction, has been found to act as an oncogene in chronic lymphocytic leukaemias and neuroendocrine prostate cancer (NEPC); however, little is known about its expression pattern, biological function, and underlying mechanism in non-small cell lung cancer (NSCLC). In this study, we observed that MIAT expression was upregulated in NSCLC, and its overexpression was associated with advanced tumor stage. Moreover, MIAT knockdown decreased cell proliferation, migration, invasion, and cell cycle arrested in G1 phase. Mechanistic investigation revealed that MIAT could interact with histone methyltransferase mixed-lineage leukemia (MLL). MIAT silencing impeded the binding of MLL on the matrix metalloproteinase 9 (MMP9) promoter region and epigenetically reduced MMP9 transcriptional activity. Overall, our findings suggest that MIAT expression is associated with NSCLC and may be one of the critical targets in progression and metastasis in NSCLC.
Highlights
Lung cancer is the leading cause of cancer-related deaths worldwide, with non-small cell lung cancer (NSCLC) accounting for approximately 85% of all cases [1]
Myocardial infarction-associated transcript (MIAT) expression was upregulated and correlated with advanced tumor stage To explore whether MIAT played a role in carcinogenesis, we first profiled the expression of MIAT in 60 pairs of nonsmall cell lung cancer (NSCLC) tissues (30 paired of adenocarcinoma and 30 paired of squamous) and paired adjacent non-tumor tissues
These results indicated that upregulated expression of MIAT might play a role in NSCLC tumorigenesis
Summary
Lung cancer is the leading cause of cancer-related deaths worldwide, with non-small cell lung cancer (NSCLC) accounting for approximately 85% of all cases [1]. The molecular mechanisms involved in the development and progression of NSCLC must be investigated. Dysregulation of lncRNAs has been reported to play a vital role in the carcinogenesis, disease progression, and metastasis of human cancers [6, 7, 10,11,12]. Some www.impactjournals.com/oncotarget lncRNAs such as H19, HOTAIR, ANRIL, MALAT1, and SCAL1 [13,14,15] have been reported to be associated with the development and progression of lung cancers. The roles of lncRNAs in NSCLC development and metastasis remain largely unknown. The identification of lung cancer-associated lncRNAs and the investigation of their molecular and biological functions in lung cancers are vital
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