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作 者:王永兴[1,2] 姜永光[1,2] 罗勇[1,2] 赵佳晖[1,2] 陈雅童[1,2] 韩毅力[1,2] 林云华[1,2]
机构地区:[1]首都医科大学附属北京安贞医院泌尿外科 [2]北京市心肺血管疾病研究所,北京100029
出 处:《首都医科大学学报》2014年第3期278-283,共6页Journal of Capital Medical University
基 金:国家自然科学基金(81341066);北京市卫生系统高层次卫生技术人才基金(2013-2-003);北京安贞医院院长科技发展基金(2013Z03)~~
摘 要:目的探讨缺氧诱导因子-1α在缺氧的条件下对前列腺癌细胞发生上皮间质转化的影响。方法在缺氧的环境中培养前列腺癌细胞PC3,并应用分子生物学的方法检测其是否是发生上皮间质转化的关键转录因子。结果缺氧微环境可以诱导前列腺癌细胞PC3发生上皮间质转化,缺氧诱导因子-1α起关键的调节作用,并且可以增强前列腺癌细胞的侵袭能力。缺氧条件下抑制缺氧诱导因子-1α的表达可以阻止前列腺癌细胞发生上皮间质转化。结论缺氧微环境通过缺氧诱导因子-1α诱导前列腺癌细胞PC3发生上皮间质转化。Objective To explore the influence of hypoxia-inducible factor-1α(HIF-1α) on prostate cancer epithelial to mesenchymal transition(EMT) under hypoxic conditions. Methods In this study we carried out several methods in molecular biology to test whether PC3, a human prostate cancer cell line, underwent typical epithelial to mesenchymal transition under hypoxia and the key regulator of this process. Results We demonstrated that hypoxia induced diverse molecular, phenotypic, and functional changes in prostate cancer cells that are consistent with EMT. We also showed that HIF-1α, which is thought to be stabilized under hypoxic environment, is involved in EMT and cancer cell invasive potency. Hypoxia-induced EMT in prostate cancer cells is blocked by HIF-1α gene silencing. Conclusion EMT may be induced in hypoxic prostate cancer cells, by a mechanism that involves activation of HIF-1α-dependent cell signaling.
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