Mechanism and Function of Angiogenin in Prostate Cancer.

Nil Vanli, H U Guo-Fu
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引用次数: 11

Abstract

Angiogenin (ANG), the fifth member of the vertebrate-specific ribonuclease (RNase) A superfamily, is a secreted angiogenic ribonuclease strongly up-regulated in human prostate cancers. ANG is translocated to the nucleus in both prostate cancer epithelial cells and endothelial cells to exert its role in prostate cancer progression by mediating tumor angiogenesis, cancer cell survival and proliferation through rRNA biogenesis. ANG-stimulated rRNA is required not only for prostate intraepithelial neoplasia (PIN) formation, but also for androgen-independent growth of prostate cancer cells. Targeting ANG by various antagonists that inhibit its nuclear translocation, function and/or activity has proven to inhibit prostate cancer growth in animal models. Furthermore, the role of ANG in androgen independence has been firmly established, suggesting a strong rationale for therapeutically targeting ANG in the treatment of castration resistant prostate cancer.

血管生成素在前列腺癌中的作用及机制。
血管生成素(Angiogenin, ANG)是脊椎动物特异性核糖核酸酶(RNase)超家族的第五个成员,是一种在人类前列腺癌中被强烈上调的分泌性血管生成核糖核酸酶。ANG在前列腺癌上皮细胞和内皮细胞中均易位至细胞核,通过rRNA生物发生介导肿瘤血管生成、癌细胞存活和增殖,在前列腺癌的进展中发挥作用。ang刺激的rRNA不仅是前列腺上皮内瘤变(PIN)形成所必需的,也是前列腺癌细胞不依赖雄激素生长所必需的。通过多种拮抗剂抑制ANG的核易位、功能和/或活性,在动物模型中已被证明可以抑制前列腺癌的生长。此外,ANG在雄激素依赖性中的作用已被明确确立,这为靶向ANG治疗去势抵抗性前列腺癌提供了强有力的理论依据。
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CiteScore
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