Overexpression of STAT4 under hypoxia promotes EMT through miR-200a/STAT4 signal pathway.

AIMS:Previous reports have found that is involved in the epithelial-mesenchymal transition (EMT), thereby regulating the metastasis and invasion of ovarian cancer. However, the mechanisms underlying remain unclear. MAIN METHODS:We first established hypoxia-induced in vivo and in vitro models. The expression levels of signal transducer and activator of transcription 4 the markers of EMT and microRNA-200a (miR-200a) were assessed by western blot and qRT-PCR analysis, respectively. Through the bioinformatics analysis and luciferase assay, the relationship between miR-200a and SATA4 was performed. The gain- and loss-function experiments were performed to examine the role of axis. KEY FINDINGS:The results showed that the protein level of duanyu18134 was significantly up-regulated in our hypoxia-exposed models, and contributed to the regulating of EMT. Besides, we found duanyu18134 was a direct target of miR-200a. Overexpression of miR-200a repressed the expression of and inhibited EMT progress, whereas the silencing of miR-200a promoted the EMT regulation both in vitro and in vivo. SIGNIFICANCE:Our results provided a potential molecular mechanism by which miR-200a involved in hypoxia-induced metastasis and invasion in ovarian cancer, suggesting a possible target for the treatment of ovarian cancer.

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