The IncRNA CCAT1 upregulates TGFβR1 via sponging miR-490-3p to promote TGFβ1-induced EMT of ovarian cancer cells

Background: Ovarian cancer is the fifth leading cause of cancer deaths in women worldwide. LncRNACCAT1 was reported to play a critical role in cell metastasis of ovarian cancer. However, little is known about the detailed mechanism of how CCAT1 enhances TGF beta 1-induced EMT of ovarian cancer cells. Methods: We used RT-qPCR to examine the level of miR-490-3p and CCAT1 and western blot to detect the protein level of TGF beta R1 and EMT-associated markers. We utilized luciferase reporter assay to confirm the direct interaction of CCAT1 or TGF beta 1 with miR-490-3p. Wound healing and invasion assay were employed to investigate the role of CCAT1 and miR-490-3p in the TGF beta 1-induced migration and cell invasion of ovarian cancer cells, respectively. Results: TGF beta 1 stimulated the expression of CCAT1. And CCAT1 knockdown decreased cell migration, invasion and EMT-associated markers expression of ovarian cancer cells treated with TGF beta 1. CCAT1 directly targeted and downregulated miR-490-3p, then increasing TGF beta R1 level. miR-490-3p was shown to regulate cell invasion, migration and EMT markers expression via TGF beta R1. In addition, we also observed that miR-490-3p was essential for TGF beta 1-induced tumor cell invasion and migration influenced by CCAT1. CCAT1 level was significantly higher in tumors than adjacent normal tissue, in contrast, miR-490-3p level was lower in ovarian tumors. Conclusion: Here, we reveal that CCAT1 contributes to TGF beta 1-induced EMT of ovarian tumor cells through miR-490-3p/TGFR1 axis. These findings will provide deep insights into the mechanism by which CCAT1 exerts its oncogenic role in ovarian cancer progression and facilitate developing novel therapeutical therapies for treating ovarian cancer.