Fig. 1

LncRNA CCAT1 depletion attenuates TGFβ1-induced EMT of ovarian cancer cells. a The level of CCAT1 in ovarian cancer cells (SKOV3 and CaOV3) was detected by RT-qPCR at 48 h after treated with TGFβ1 (10 ng/ml). b RT-qPCR analysis was performed to confirm target gene CCAT1 silencing after shRNA treatment. RNA level of CCAT1 in sh-NC (scramble) and sh-CCAT1 (CCAT1 knockdown) were detected in ovarian cancer cells (SKOV3 and CaOV3). c, d Representative images of wound healing assay (c) and quantification (d) carried out in control (wildtype), sh-NC (scramble) and sh-CCAT1 (CCAT1 knockdown) ovarian cancer cells (SKOV3 and CaOV3) treated with 10 ng/ml TGFβ1. e Cell invasion ability of control (wildtype), sh-NC (scramble) and sh-CCAT1 (CCAT1 knockdown) ovarian cancer cells (SKOV3 and CaOV3) was measured with transwell invasion assay under 10 ng/ml TGFβ1. f the mRNA level of EMT-associated markers (claudin, E-cadherin, N-cadherin, vimentin and MMP9) in control (wildtype), sh-NC (scramble) and sh-CCAT1 (CCAT1 knockdown) ovarian cancer cells (SKOV3 and CaOV3) was measured by RT-qPCR analysis after cells treated with 10 ng/ml TGFβ1. g Western blot analysis showed the protein level of EMT-associated markers (claudin, E-cadherin, N-cadherin, vimentin and MMP9) after cells were transfected with sh-CCAT1 (CCAT1 knockdown) in ovarian cancer cells (SKOV3 and CaOV3) compared with the control (wildtype), sh-NC (scramble) groups under with 10 ng/ml TGFβ1. All data were represented as mean ± SD from three biological replicates (*P < 0.05; **P < 0.01)