MicroRNA-204 inhibits cell migration and invasion in human cervical cancer by regulating transcription factor 12.

Deregulated microRNAs (mills) and their roles in carcinogenesis have attracted great attention in recent years. Although miR-204 was reportedly dysregulated in various types of cancer, its function and mechanism in cervical cancer remain unknown. The present study focused on the expression and mechanisms of miR-204 in cervical cancer development. Expression of miR-204 in cervical cancer tissues and non-tumor tissues was measured using PCR analysis. The effect of ectopic expression of miR-204 on cell motility was evaluated using wound-healing and Transwell invasion assays. Luciferase activity and western blot assays were used to verify the regulatory effect of miR-204 on its target gene. It was demonstrated that miR-204 was significantly decreased in primary cervical cancer tissues, and that downregulated miR-204 was associated with lymph node metastasis and poor survival. In addition, it was revealed that ectopic expression of miR-204 significantly inhibited the migratory and invasive ability of cervical cancer cells in vitro. In addition, bioinformatic prediction and experimental validation demonstrated that transcription factor 12 (TCF12) was a direct target of miR-204. Overexpression of TCF12 attenuated the inhibitory effect of miR-204 on cell motility. Taken together, the present data indicated that miR-204 is a metastasis-associated gene and may contribute to the progression of cervical cancer by regulating TCF12, providing novel insights, including that miR-204/TCF12 may be an important mechanism for cervical cancer metastasis.