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. 2019 Jun 12;44(2):683–693. doi: 10.3892/ijmm.2019.4241

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Copyright: © Liu et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Celecoxib inhibits the epithelial-to-mesenchymal transition and upregulates miR-145 in bladder cancer cells. 5637 and T24 bladder cancer cells were treated with DMSO or celecoxib (60 or 80 µM) for 48 h. (A) Protein expression of COX-2 in 5637 and T24 cells subsequent to treatment with celecoxib were detected by western blot analysis. GAPDH was used as an internal control. (B) mRNA expression levels of E-cadherin and Vimentin were examined using RT-qPCR. GAPDH was used as an internal control. (C) Protein expression levels of E-cadherin and Vimentin in 5637 and T24 cells were detected by western blot analysis and (D) quantified. GAPDH was used as an internal control. Celecoxib inhibits the epithelial-to-mesenchymal transition and upregulates miR-145 in bladder cancer cells. (E) Expression levels of miR-145 in bladder cancer cell lines, as detected by RT-qPCR. SV-HUC-1 was used as a normal control. Effect of celecoxib on the expression levels of miR-145 in (F) dose-dependent and (G) time-dependent manners. Expression levels of miR-145 in 5637 and T24 cells following treatment with celecoxib were detected by RT-qPCR. U6 was used as an internal control. The data represent the mean ± standard deviation of three independent experiments. ^**P<0.05 vs. the DMSO group. DMSO, dimethyl sulfoxide; COX2, cyclooxygenase-2; miR, microRNA; RT-qPCR, reverse transcription-quantitative polymerase chain reaction.

Celecoxib inhibits the epithelial-to-mesenchymal transition and upregulates miR-145 in bladder cancer cells. 5637 and T24 bladder cancer cells were treated with DMSO or celecoxib (60 or 80 µM) for 48 h. (A) Protein expression of COX-2 in 5637 and T24 cells subsequent to treatment with celecoxib were detected by western blot analysis. GAPDH was used as an internal control. (B) mRNA expression levels of E-cadherin and Vimentin were examined using RT-qPCR. GAPDH was used as an internal control. (C) Protein expression levels of E-cadherin and Vimentin in 5637 and T24 cells were detected by western blot analysis and (D) quantified. GAPDH was used as an internal control. Celecoxib inhibits the epithelial-to-mesenchymal transition and upregulates miR-145 in bladder cancer cells. (E) Expression levels of miR-145 in bladder cancer cell lines, as detected by RT-qPCR. SV-HUC-1 was used as a normal control. Effect of celecoxib on the expression levels of miR-145 in (F) dose-dependent and (G) time-dependent manners. Expression levels of miR-145 in 5637 and T24 cells following treatment with celecoxib were detected by RT-qPCR. U6 was used as an internal control. The data represent the mean ± standard deviation of three independent experiments. ^**P<0.05 vs. the DMSO group. DMSO, dimethyl sulfoxide; COX2, cyclooxygenase-2; miR, microRNA; RT-qPCR, reverse transcription-quantitative polymerase chain reaction.