CAJ | 학술논문

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。
목적：탐토결양유도인자-1α재결양적조건하대전렬선암세포발생상피간질전화적영향。방법재결양적배경중배양전렬선암세포 PC3,병응용분자생물학적방법검측기시부시발생상피간질전화적관건전록인자。결과결양미배경가이유도전렬선암세포 PC3발생상피간질전화,결양유도인자-1α기관건적조절작용,병차가이증강전렬선암세포적침습능력。결양조건하억제결양유도인자-1α적표체가이조지전렬선암세포발생상피간질전화。결론결양미배경통과결양유도인자-1α유도전렬선암세포 PC3발생상피간질전화。
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.