Objective To investigate the co-transfection of p53 and angiostatin gene in the inhibition of SG7901. Methods Transfected the pVITRO2-hp53-hAS into SG7901 with lipofectamine.After transfection, RT-PCR were used to know whether the aimed gene had been transfected and expressed or not. Cell clones trial, MTT growth curve, cell cycle measuring were used to analyze the differences. Results The cells were suppressed by the two genes and inhibition of the combined genes is more powerful than single one. Conclusion The effection of combined genes pVITRO2-hp53-hAS on SG7901 is stronger than either single one. Combined-gene-therapy is a useful anti-carcinoma method.

Objective To investigate the mechanism of EMT and invasion promoted by miR-21 in prostate cancer cells. Methods The sequence of miR-21 mimic/inhibitor was firstly designed and synthesized. Then miR-21 mimic/inhibitor and its control were transfected into prostate cancer cells C4-2 and DU145, respectively. And cells were collected for mRNA isolation and RT-qPCR analysis for miR-21 and FOXOl. FOXOl, E-cadherin and N-cadherin were detected by Western blot, and the invasion of prostate cancer cells were detected by transwell assays. Results The expression of miR-21 increased in both C4-2 and DU145 after transfection, and the expression of FOXOl mRNA increased at the same time (P＜0.01).The expression of miR-21 and FOXOl mRNA in C4-2 and DU145 was decreased by miR-21 inhibitor(P＜ 0.05). The protein expression of FOXOl and N-cadherin in C4-2 and DU145 increased after the treatment of miR-21, while that of E-cadherin decreased. The protein expression of FOXOl and N-cad-herin in C4-2 and DU145 decreased after the treatment of miR-21 inhibitor, while that of E-cadherin increased. The invasive level in C4-2 and DU145 increased after the treatment of miR-21, while that decreased after the treatment of miR-21 inhibitor. Conclusion MiR-21 promotes EMT and invasion by inducing FOXOl in prostate cancer cells.