Fig 2: RNF7 knockdown inhibited cell proliferation.Cell numbers of DU145 (a) and PC3 (b) transfected with shCON or shRNF7-2 were monitored for 7 days. Data were mean ± SD. **P < 0.01; ***P < 0.001.

Fig 3: RNF7 knockdown induced cell growth inhibition.(a) Expression of pro-apoptosis protein NOXA and tumor suppressor proteins p21 and p27 was detected by western blot assay. shRNF7-1 or shRNF7-2: cells interfered by shRNF7-1 or shRNF7-2 retrovirus. (b) Both shRNF7-2 interfered (shRNF7-2 group) or the negative control (shCON group) prostate cells were stimulated with EGF for 5 to 60 minutes, and expression or phosphorylation of ERK was detected by Western blot assay.

Fig 4: RNF7 expression was efficiently inhibited by shRNA interference.Prostate cancer cells were transfected with shRNF7-1, shRNF7-2 retrovirus or shCON negative control retrovirus. RNF7 expression was assessed by western blot (a), and confirmed on qRT-PCR (b). Results were representatives of three independent experiments. Data were mean ± SD. ***P < 0.001.

Fig 5: RNF7 knockdown inhibited prostate tumorigenesis.Colonies formed by DU145 (a) and PC3 (b) shRNA interfered cells (shRNF7-2 group) were significantly lower than those formed by negative controls (shCON group). DU145 (c) or PC3 cells (d) (both shNRF7 interfered and shCON negative controls) were implanted subcutaneously into the back of nude mice. Each group contained 6 nude mice. Mice were sacrificed six weeks later. Xenografts were collected and their weights were measured. Representative photos and statistical data were showed. Data were mean ± SD. ***P < 0.001.