Fig. 5: Knockdown of RFC3 partially attenuated the growth advantage and DNA damage repair capability incurred by BTF3b-overexpression. | Cell Death & Disease

Fig. 5: Knockdown of RFC3 partially attenuated the growth advantage and DNA damage repair capability incurred by BTF3b-overexpression.

From: BTF3 confers oncogenic activity in prostate cancer through transcriptional upregulation of Replication Factor C

Fig. 5

a, b Relative cell growth of DU145 and PC-3 prostate cancer cells with or without ectopic BTF3a (a) or BTF3b (b) overexpression. Mean ± S.D. for three independent experiments are shown. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001 (Student’s t-test). c qRT-PCR analysis of the RFCs mRNA levels was conducted in DU145 (left panel) and PC-3 (right panel) prostate cancer cells with or without ectopic BTF3b overexpression. d qRT-PCR analysis of RFC3 mRNA levels was conducted in DU145 cells as indicated. ACTB was used as an endogenous control. Data are shown as mean ± S.D. from three independent experiments. **p < 0.01, ***p < 0.001, ****p < 0.0001 (Student’s t-test). e Relative cell growth of prostate cancer cells as in d. Data are shown as mean ± S.D. for three independent experiments. ***p < 0.001 (Student’s t-test). f The effect of RFC3 silencing on the extent of DNA damage in BTF3b-overexpressing DU145 cells was measured by alkaline comet assay. Cells were harvested at the indicated time points after a 30-min treatment with H2O2 (100 μM). Scale bar, 50 μm. Quantification of DNA in the tail is shown as mean ± SD. ***p < 0.001 (Student’s t-test).

Back to article page