目的：探讨SOX10对前列腺癌细胞增殖及侵袭能力的影响。方法：利用Western blotting方法检测SOX10蛋白在前列腺癌细胞系PC3、DU145及LNcap中的表达水平。利用si-RNA干扰的方法下调前列腺癌细胞系PC3及DU145中SOX10的表达，通过细胞增殖及侵袭实验评估SOX10对前列腺癌细胞增殖能力和侵袭能力的影响。结果：下调SOX10后，前列腺癌细胞的增殖能力明显降低，表现为实验组中前列腺癌细胞PC3及DU145的光密度值明显低于对照组（细胞系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。细胞系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）；同时，下调SOX10后前列腺癌细胞的侵袭能力也明显受到抑制，与对照组相比，实验组迁出的细胞数明显减少(细胞系PC3: 142±38, 171±17 vs. 304±55; 细胞系DU145：96±22, 134±23 vs. 341±34)， 差异均具有统计学意义（P均<0.05）。结论：SOX10可能通过促进前列腺癌细胞的增殖和侵袭能力促进前列腺癌的发生及进展，并且可能成为前列腺癌潜在的治疗靶点。

Objective： To explore the influence of SOX10 on the proliferation and invasion of prostate cancer cells. Methods: SOX10 protein in prostate cancer cell lines PC3, DU145 and LNcap was detect-ed 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. Results: 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). Conclusions: 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.