低氧对前列腺癌PC3细胞上皮间质转化的影响

 目的 探讨低氧对前列腺癌细胞上皮间质转化的影响。方法 分别在常氧（常氧组）和低氧（低氧组）条件下培养PC3细胞24 h，细胞增殖MTT实验检测低氧对前列腺癌PC3细胞增殖力的影响，Transwell侵袭实验评估低氧对前列腺癌PC3细胞侵袭力的影响，Western blot检测HIF-1α、E-cadherin、N-cadherin和Vimentin的表达水平。另外，在常氧条件下用siRNA抑制HIF-1α表达（干扰组），用Western blot检测E-cadherin、N-cadherin和Vimentin的表达水平变化。结果 与常氧组比较，低氧组前列腺癌PC3细胞的增殖力和侵袭力增加，HIF-1α表达水平增加（P=0.0004），HIF-1α向核内转位；N-cadherin（P<0.0001）和Vimentin（P<0.0001）的表达水平显著增加，E-cadherin的表达水平显著下降（P<0.0001）。同时，干扰组跟常氧组比较，抑制HIF-1α表达使N-cadherin（P=0.0002）和Vimentin（P=0.0002）的表达水平显著下降，而使E-cadherin的表达水平显著增加（P<0.0001）。结论 低氧可能通过调节HIF-1α表达促进前列腺癌PC3细胞的上皮间质转化。

Effect of Hypoxia on Epithelia-mesenchymal Transition of Prostate Cancer PC3 Cells

jective To investigate the effect of hypoxia on epithelia-mesenchymal transition of prostate cancer cells PC3. Methods PC3 cells were cultured under aerobic condition (Normal group) and hypoxia condition (Hypoxia group) for 24 h, respectively. Then, the ability of proliferation was detected by MTT, the ability of invasion was assayed by Transwell, and the protein expressions of HIF-1α, E-cadherin, N-cadherin and Vimentin were assayed by Western blot. Meanwhile, PC3 cells were treated with siRNA to inhibit expression of HIF-1α under aerobic condition and then the protein expressions of HIF-1α E-caldherin, N-cadherin and Vimentin were assayed by Western blot.Results Compared with Normal group, the abilities of cell invasion and proliferation were significantly enhanced by hypoxia; and the protein expressions of HIF-1α(P=0.0004), N-cadherin(P<0.0001) and Vimentin(P<0.0001) were significantly increased, but the protein expression of E-cadherin(P<0.0001) was significantly decreased in Hypoxia group; meanwhile, hypoxia promoted HIF-1α to translocate to nucleus.Furthermore, compared with normal group, inhibition expression of HIF-1α by siRNA significantly decreased the protein expressions of N-cadherin(P=0.0002) and Vimentin(P=0.0002), but significantly increased the protein expression of E-cadherin(P<0.0001). Conclusion Hypoxia might promote epithelia-mesenchymal transition of prostate cancer cells PC3 via regulating the expression of HIF-1α.