Tang X, Zhao W H, Song Q Q, Yin H Q, DU Y Q, Sheng Z Z, Wang Q, Zhang X W, Li Q, Liu S J
Department of Urology, Peking University People's Hospital, Beijing 100044, China.
Department of Urology, Weinan City Center Hospital, Weinan 714000, Shaanxi, China.
Beijing Da Xue Xue Bao Yi Xue Ban. 2018 Aug 18;50(4):602-606.
To explore the influence of SOX10 on the proliferation and invasion of prostate cancer cells.
SOX10 protein in prostate cancer cell lines PC3, DU145 and LNcap was detected by Western blotting analysis. The expression of SOX10 in prostate cancer cell lines (PC3 and DU145) were knocked down by small interfering RNAs, and the efficiency of SOX10 by small interfering RNAs was confirmed using Western blotting analysis. CCK-8 assays were conducted to assess the influences of SOX10 on the proliferation of PC3 and DU145 cells, and invasion assays were conducted to assess the influences of SOX10 on the invasion of PC3 and DU145 cells.
After SOX10 in prostate cancer cells was knocked down by small interfering RNAs, the proliferation of prostate cancer cells PC3 and DU145 was significantly inhibited. Results of CCK-8 assays showed that the absorbance of PC3 and DU145 in SOX10-silenced groups was decreased compared with those in control groups (PC3: 0 d: 0.166±0.01, 0.162±0.012 vs. 0.155 ±0.01, P>0.05; 1 d: 0.210±0.011, 0.211±0.018 vs. 0.252±0.023, P>0.05; 2 d: 0.293±0.017, 0.280±0.028 vs. 0.433±0.030, P<0.01; 3 d: 0.363±0.071, 0.411±0.038 vs. 0.754±0.045, P<0.01; 4 d: 0.592±0.065, 0.670±0.093 vs. 1.456±0.111, P<0.01. DU145: 0 d: 0.168±0.018, 0.164±0.01 vs. 0.153 ±0.012, P>0.05; 1 d: 0.218±0.007, 0.206±0.024 vs. 0.255±0.02, P>0.05; 2 d: 0.297±0.013, 0.291±0.012 vs. 0.444±0.023, P<0.05; 3 d: 0.378±0.058, 0.419±0.026 vs. 0.762±0.039, P<0.01; 4 d: 0.681±0.094, 0.618±0.050 vs. 1.419±0.170, P<0.01). Meanwhile, knocking down SOX10 significantly suppressed the invasion of prostate cancer cells PC3 and DU145. Results of invasion assays showed that the numbers of invaded cells in SOX10-silenced groups were significantly less than those in control groups (PC3: 142±38, 171±17 vs. 304±55; DU145: 96±22, 134±23 vs. 341±34, P<0.05).
SOX10 might promote prostate cancer progression by accelerating the ability of the proliferation and invasion of prostate cancer cells, and SOX10 might be a potential therapeutic target for prostate cancer.
探讨SOX10对前列腺癌细胞增殖和侵袭的影响。
采用蛋白质免疫印迹分析检测前列腺癌细胞系PC3、DU145和LNcap中SOX10蛋白。用小干扰RNA敲低前列腺癌细胞系（PC3和DU145）中SOX10的表达，并通过蛋白质免疫印迹分析确认小干扰RNA对SOX10的敲低效率。进行CCK-8试验以评估SOX10对PC3和DU145细胞增殖的影响，并进行侵袭试验以评估SOX10对PC3和DU145细胞侵袭的影响。
用小干扰RNA敲低前列腺癌细胞中的SOX10后，前列腺癌细胞PC3和DU145的增殖受到显著抑制。CCK-8试验结果显示，与对照组相比，SOX10沉默组中PC3和DU145的吸光度降低（PC3：0天：0.166±0.01，0.162±0.012对0.155±0.01，P>0.05；1天：0.210±0.011，0.211±0.018对0.252±0.023，P>0.05；2天：0.293±0.017，0.280±0.028对0.433±0.030，P<0.01；3天：0.363±0.071，0.411±0.038对0.754±0.045，P<0.01；4天：0.592±0.065，0.670±0.093对1.456±0.111，P<0.01。DU145：0天：0.168±0.018，0.164±0.01对0.153±0.012，P>0.05；1天：0.218±0.007，0.206±0.024对0.255±0.02，P>0.05；2天：0.297±0.013，0.291±0.012对0.444±0.023，P<0.05；3天：0.378±0.058，0.419±0.026对0.762±0.039，P<0.01；4天：0.681±0.094，0.618±0.050对1.419±0.170，P<0.01）。同时，敲低SOX10显著抑制了前列腺癌细胞PC3和DU145的侵袭。侵袭试验结果显示，SOX10沉默组中侵袭细胞的数量明显少于对照组（PC3：142±38，171±17对304±55；DU145：96±22，134±23对341±34，P<0.05）。
SOX10可能通过加速前列腺癌细胞的增殖和侵袭能力促进前列腺癌进展，且SOX10可能是前列腺癌的一个潜在治疗靶点。
