miR-203a regulates bladder cancer cell proliferation and radiosensitivity by targeting CDK6 / 中华放射肿瘤学杂志

Objective:To investigate the expression of miR-203a in bladder cancer (BC) cell lines (RT-112, T24, 5637, UM-UC-3) and evaluate the effects on BC cell proliferation and radiosensitivity.Methods:Mir-203a mimics, mir-203a inhibitor, CDK6 siRNA, CDK6 expression plasmid and corresponding negative controls were transfected into BC cells. Quantitative real-time PCR was used to detect the expression of miR-203a in BC cell lines and human bladder epithelial immortalized cell line (SV-HUC-1). CCK8 assay was used to investigate the regulation of miR-203a and cyclin-dependent kinases 6(CDK6) on the proliferation of BC cells. Colony formation assay was performed to assess the effect of miR-203a and CDK6 on the radiosensitivity of BC cells. The target gene of miR-203a was confirmed by luciferase reporter assay. The effect of miR-203a on CDK6 protein expression was detected by Western blot. Multi-group comparison was performed by one-way ANOVA and two-group comparison was conducted by t-test. Results:Compared with the SV-HUC-1 cells, the expression levels of miR-203a in RT-112, T24, 5637 and UM-UC-3 cells were significantly down-regulated (all P<0.05). Compared with NC group, overexpression of miR-203a significantly inhibited the proliferation of BC cells, whereas knockdown of miR-203a significantly promoted the proliferation of BC cells (both P<0.05). Compared with NC group, overexpression of miR-203a significantly increased the sensitivity of BC cells to radiotherapy, whereas knockdown of miR-203a significantly weakened the sensitivity of BC cells to radiotherapy (both P<0.05). CDK6 was the target of miR-203a. Compared with NC group, overexpression of miR-203a significantly down-regulated the expression level of CDK6 protein, whereas knockdown of miR-203a significantly up-regulated the expression level of CDK6 protein (both P<0.05). After overexpression of CDK6 in T24 and UM-UC-3 cells transfected with miR-203a mimics, the cell proliferation ability was significantly increased, whereas the sensitivity to radiotherapy was significantly decreased compared with mir-203a mimics (both P<0.05). After CDK6 was silenced in RT-112 and 5637 cells transfected with miR-203a inhibitor, the proliferation ability of cells was significantly decreased, whereas the sensitivity to radiotherapy was remarkably increased compared with miR-203a inhibitor group (both P<0.05). Conclusion:miR-203a can serves as a tumor suppressor gene to inhibit the proliferation of BC cells and enhance the radiosensitivity of BC cells.

Randomized trial on late course accelerated hyperfractionation radiotherapy for squamous cell carcinoma of upper and mid-thoracic esophagus / 中华放射肿瘤学杂志

0.05). The incidence of acute esophagitis was increased but it was acceptable in the LACF group (P