Abstract
The present study aimed to explore the biological functions and mechanism of long non-coding RNA myocardial infarction-associated transcript (MIAT) in melanoma progression. MIAT expression in melanoma tissue samples and cells was detected by quantitative real-time PCR. After gain-of-function and loss-of-function models were constructed, cell counting kit-8, EdU, and Transwell assays were employed to detect the proliferation, migration, and invasion of melanoma cells. catRAPID database was employed and RNA pull-down assay and RNA immunoprecipitation assay were utilized to verify, the binding relationship between MIAT and transcription factor 12 (TCF12). The binding of TCF12 to the promoter region of the gene of nuclear factor of activated T cells 5 (NFAT5) was verified by chromatin immunoprecipitation-quantitative PCR assay and dual-luciferase reporter gene assay. The regulatory effects of MIAT and TCF12 on NFAT5 expression were detected via Western blot. The results showed that MIAT expression was increased in melanoma tissues and cells, and was significantly associated with the AJCC stage and the differentiation of melanoma tissues. MIAT overexpression markedly facilitated melanoma cells' multiplication, migration, and invasion, while MIAT knockdown inhibited the multiplication, migration, and invasion. MIAT showed direct interaction with TCF12. MIAT promoted the binding of TCF12 to NFAT5 promoter region, thereby promoting NFAT5 transcription. In conclusion, MIAT promotes melanoma progression through recruiting TCF12 and its interaction with NFAT5.