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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 TGFβ1-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 TGFβR1 and EMT-associated markers. We utilized luciferase reporter assay to confirm the direct interaction of  CCAT1  or TGFβ1 with  miR - 490 - 3p . Wound healing and invasion assay were employed to investigate the role of  CCAT1  and  miR - 490 - 3p  in the TGFβ1-induced migration and cell invasion of ovarian cancer cells, respectively.    Results  TGFβ1 stimulated the expression of CCAT1. And CC AT1  knockdown decreased cell migration, invasion and EMT-associated markers expression of ovarian cancer cells treated with TGFβ1.  CCAT1  directly targeted and downregulated  miR - 490 - 3p , then increasing TGFβR1 level.  miR - 490 - 3p  was shown to regulate cell invasion, migration and EMT markers expression via TGFβR1. In addition, we also observed that  miR - 490 - 3p  was essential for TGFβ1-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 TGFβ1-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.

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