Circ_0067835 sponges miR-324-5p to induce HMGA1 expression in endometrial carcinoma cells.

Endometrial cancer is a common gynaecological malignant tumour among women across the world. Circular RNAs (circRNAs) are a novel kind of non-coding RNAs, and they can play a crucial role in multiple cancers. Nevertheless, the mechanisms of circRNAs in regulating gene expression in endometrial cancer are still unclear. Here, our work sought to focus on the role that circ_0067835 exert in progression and development of endometrial cancer cells. We observed circ_0067835 was markedly elevated in endometrial cancer. Then, changes in endometrial cancer cell (RL95-2 and HEC-1B) function were determined after circ_0067835 knockdown. Loss-of-functional assays revealed that circ_0067835 down-regulation significantly repressed RL95-1 and HEC-1B cell proliferation, migration and invasion. Bioinformatics analysis, luciferase reporter experiment and RNA pull-down assay were employed to predict and validate circ_0067835 can bind to miR-324-5p. Increase in miR-324-5p remarkably depressed the proliferation, migration and invasion of endometrial cancer cells via inhibiting high mobility group A1 (HMGA1). HMGA1 is identified as a vital prognostic biomarker in endometrial cancer. Currently, we reported circ_0067835 was positively correlated with HMGA1 in endometrial cancer. We implied that circ_0067835 was capable of sponging miR-324-5p and inducing its downstream target HMGA1 in vitro and in vivo. In conclusion, circ_0067835 can compete with miR-324-5p, resulting in HMGA1 up-regulation, and therefore induce the development of endometrial cancer.