The
nuclear factor I/X (NFIX) plays important roles in cell differentiation, but its function in
cancer is still unclear. Besides, accumulating studies reported the important role of
microRNAs (
miRNAs) in the regulation of gene expression, among of which, the miR-1290 has been widely reported in various
cancers. In this study, we investigated the mechanism through which NFIX was regulated by
miRNAs. Firstly, we found that the NFIX
protein and
mRNA levels were consistently down-regulated in ESCC tissues suggesting that a post-transcriptional mechanism maybe involved in the regulation of NFIX. Since
microRNAs (
miRNAs) are powerful post-transcriptional regulators of gene expression, we performed bioinformatic analyses to search for
miRNAs that potentially target NFIX. We identified the specific targeting site of miR-1290 in the 3'-UTR of NFIX and the inverse correlation between the levels of miR-1290 and NFIX
protein and
mRNA in ESCC tissue samples was then confirmed. By overexpressing or silencing miR-1290 in ESCC cells, we experimentally validated that miR-1290 directly binds to the 3'-UTR of the NFIX transcript and degrade the NFIX
mRNA to regulate NFIX expression. Furthermore, the
biological consequences that miR-1290 mediated by targeting NFIX were examined in vitro. We demonstrated that miR-1290 could promote proliferation, migration and invasion via the negative regulation of NFIX expression. Taken together, our findings suggested that miR-1290 functions as a
tumor oncogene in the progression of ESCC by targeting NFIX.