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缺氧诱导因子-1α与前列腺癌生物学行为的关系 被引量:6

Relationship between the expression of hypoxia inducible factor-1 α and biological behavior of prostate cancer
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摘要 目的探讨缺氧诱导因子1α(HIF1α)与前列腺癌侵袭转移、分化增殖及凋亡的关系。方法采用免疫组化方法检测40例前列腺癌和10例前列腺增生(BPH)中HIF1α与增殖细胞核抗原(PCNA)、B细胞淋巴瘤基因2(Bcl2)、CD34的表达及计算微血管密度(MVD)。结果前列腺癌中HIF1α的表达明显高于BPH;HIF1α在前列腺癌中的表达水平与前列腺癌的病理分级和临床分期均呈正相关;前列腺癌中HIF1α的表达与PCNA及MVD呈正相关,与Bcl2呈负相关。结论HIF1α水平升高在前列腺癌的发生、发展过程中可能起重要作用;HIF1α的表达水平可用于预测前列腺癌的生物学行为,可作为前列腺癌治疗的新靶点。 Objective To determine the relationship between the expression of hypoxia inducible factor-1α(HIF-1α)and the invasion,metastasis,pathological grade,proliferation,and apoptosis in prostate cancer.Methods HIF-1α,PCNA,Bcl-2,and CD34 were detected by immunohistochemistry method in the tissues of 40 cases with prostate cancer and 10 cases with BPH.Results HIF-1α levels in prostate were much higher than those in BPH.The degree of cancer malignancy and invasion was positively correlated with the expression of HIF-1α.HIF-1α level was positively correlated with the expression of PCNA and MVD and negatively correlated with Bcl-2 level.Conclusion HIF-1α might play an important role in the carcinogenesis and progression of prostate cancer.HIF-1α level can be used to predict biological behavior and be a new treatment target of prostate cancer.
出处 《江苏医药》 CAS CSCD 北大核心 2005年第7期489-491,共3页 Jiangsu Medical Journal
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  • 1Zhong H, De Marzo AM, Laughner E, et al. Overexpression of hypoxia-inducible factor-1 alpha in common human cancers and their metastases. Cancer Research, 1999,59: 5830-5835.
  • 2Semenza GL, Agani F, Feldser D, et al. Hypoxia, HIF-1 and the pathophysiology of common human diseases. Adv Exp Med Biol, 2000,475:123-130.
  • 3Iervolino A, Trisciuoglio D, Ribatti D, et al. Bcl-2 overexpression in human melanoma cells increases angiogenesis through VEGF mRNA stabilization and HIF-1-mediated transcriptional activity.FASEB J, 2002,16:1453-1455.
  • 4Iida T, Mine S, Fujimoto H, et al. Hypoxia-inducible factor-1 alpha induces cell cycle arrest of endothelial cells. Genes Cells,2002,7:143-149.

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