Research Paper Volume 13, Issue 14 pp 18527—18544

LncRNA CCAT1 promotes prostate cancer cells proliferation, migration, and invasion through regulation of miR-490-3p/FRAT1 axis

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Figure 6. miR-490-3p inhibition restored the influences of CCAT1 knockdown in PCa cells. (A) miR-490-3p expression in LnCaP and PC3 cells transfected with si-CCAT1 or si-CCAT1+miR-inhibitor. (B) Cell viability of LnCaP and PC3 cells with different treatments. Cell viability was suppressed by down-regulation of CCAT1, and reversed by additional treatment with miR-inhibitor. (C) EdU staining results in each group of LnCaP and PC3 cells. Cell proliferation inhibition induced by si-CCAT1 was alleviated by additional treatment with miR-inhibitor. Scale bar: 50 μm. (D) Cell apoptosis of LnCaP and PC3 cells by flow cytometry detection. Cell apoptosis was increased by si-CCAT1 transfection and reactivated after miR-490-3p inhibition. (E, F) Cell migration and invasion of LnCaP and PC3 cells by Transwell assays. Cell migration and invasion in PCa cells were blocked in si-CCAT1 group and retrieved in si-CCAT1+miR-inhibitor group. (G) Down-regulation of CCAT1 increased the expression of E-cadherin yet decreased N-cadherin and Vimentin expression, and this effect was retrieved in the si-CCAT1+miR-inhibitor group. *P < 0.05, **P < 0.01, compared with the si-NC group; #P < 0.05, ##P < 0.01, compared with the si-CCAT1 group.