Prolyl hydroxylase-2 (PHD2)施加在胰腺癌肿瘤抑制活动。
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苏Y,厕所,Giese N, Metzen E, Buchler MW,薯条H P的科恩伯格,•巴克勒
Prolyl hydroxylase-2 (PHD2)施加在胰腺癌肿瘤抑制活动。
癌症。2012年2月15日,118 (4):960 - 72。doi: 10.1002 / cncr.26344。Epub 2011年7月26日。
- PubMed ID
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21792862 (在PubMed]
- 文摘
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背景:最常见的胰腺癌是1和治疗肿瘤。寻找新的治疗方法,氧传感器prolyl羟化酶(博士)是潜在的目标。PHD2被认为是关键的氧气sensor-regulating低氧诱导因子(HIF)。目前,有相互矛盾的证据关于确切的PHD2在肿瘤发生中的作用。本研究的目的是调查在胰腺癌PHD2增长和发展的作用。方法:分析了PHD2表达式定量实时聚合酶链反应分析和免疫组织化学在人类组织标本和细胞系。击倒PHD2是由使用short-interfering rna (siRNAs)具体对PHD2和PHD2超表达是通过稳定组合DNA转染。体内,原位使用小鼠模型。血管生成细胞因子进行评估与酶联免疫吸附实验,研究了入侵与基底膜基质化验。结果:PHD2表达并没有显著改变在癌症组织和转移。 Lymph node-negative tissues had higher levels of PHD2 than lymph node-positive tissues. PHD2 was hypoxia-inducible in pancreatic cancer cell lines and regulated cell growth through cyclin D1 down-regulation samples with PHD2 suppression and through p21 up-regulation in samples with of PHD2 overexpression. In vivo, PHD2 caused tumor growth retardation and reduced tumor invasion by inhibiting angiogenesis. This observation was caused by the suppression of angiogenic cytokines and tumor invasion. CONCLUSIONS: The current results indicated that PHD2 plays an important role in pancreatic tumorigenesis. In summary, the authors concluded that PHD2 may function as a tumor suppressor gene in pancreatic cancer and, thus, may define a potential target for the treatment of pancreatic cancer.