Immunohistochemical analysis of Omi/HtrA2 expression in prostate cancer and benign prostatic hyperplasia
Immunohistochemical analysis of Omi/HtrA2 expression in prostate cancer and benign prostatic hyperplasia
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DOI：
10.1111/j.1600-0463.2006.apm_271.x
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发表时间：
2006-12-01
期刊：
影响因子：
2.8
通讯作者：
Zeng, Fu-Qing
中科院分区：
文献类型：
--
作者：
Hu, Xiao-Yong;Xu, Yue-Min;Zeng, Fu-Qing
丝氨酸蛋白酶Omi/HtrA2在凋亡刺激后从线粒体释放到细胞质中，通过其蛋白酶活性以caspase独立的方式诱导细胞凋亡，并通过中和凋亡抑制蛋白（IAPs）对caspase的抑制以caspase依赖的方式诱导细胞凋亡。细胞凋亡的改变对癌症的发展至关重要，而放化疗导致的癌细胞死亡在很大程度上依赖于细胞凋亡。因此，分析细胞凋亡调控因子Omi/HtrA2在肿瘤组织中的表达状况，是了解肿瘤发生的必要条件。本研究采用免疫组化方法对65例前列腺癌、40例良性前列腺增生和10例正常前列腺标本中Omi/HtrA2的表达进行了分析。采用半定量逆转录聚合酶链反应检测前列腺癌和良性前列腺增生组织体内Omi/HtrA2 mRNA水平。Omi/HtrA2在大多数前列腺癌中呈免疫阳性（定义为>= 30%），高分化组的Omi/HtrA2阳性率低于低分化组和中分化组（p < 0.005）。而在正常前列腺和良性前列腺增生组细胞中，Omi/HtrA2不表达或仅弱表达。前列腺癌组织中Omi/HtrA2 mRNA表达水平明显高于良性前列腺增生组织（p < 0.001）。综上所述，这些结果提示体内前列腺癌细胞的凋亡可能需要Omi/HtrA2的表达，而Omi/HtrA2的表达可能参与了前列腺癌的发展。
The serine protease Omi/HtrA2 is released from mitochondria into the cytosol after apoptotic stimuli, inducing apoptosis in a caspase-independent manner through its protease activity and in a caspase-dependent manner by neutralizing the inhibition of inhibitor of apoptosis proteins (IAPs) on caspases. Alteration of apoptosis is essential for cancer development, and cancer cell death by radiation and chemotherapy is largely dependent upon apoptosis. Thus, analysis of the expression status of Omi/HtrA2, a regulator of apoptosis, in cancer tissues is needed for an understanding of cancer development. In the current study we analyzed the expression of Omi/HtrA2 in 65 prostate cancer, 40 benign prostatic hyperplasia and 10 normal prostate specimens by immunohistochemistry. Omi/HtrA2 mRNA levels of in vivo prostate cancer and benign prostatic hyperplasia samples were also assayed by semiquantitative reverse transcription-polymerase chain reaction. Immunopositivity (defined as >= 30%) was observed for Omi/HtrA2 in most of the prostate cancers, and the positive rate of Omi/HtrA2 was lower in the well-differentiated group than in the poorly and moderately differentiated groups (p < 0.005). By contrast, the cells in the normal prostate and benign prostatic hyperplasia groups showed no or only weak expression of Omi/HtrA2. Meanwhile, the Omi/HtrA2 mRNA level of prostate cancer is much higher than that of benign prostatic hyperplasia (p < 0.001). Taken together, these results suggest that prostate cancer cells in vivo may need Omi/HtrA2 expression for apoptosis, and that Omi/HtrA2 expression might be involved in prostate cancer development.