Suppr超能文献

雄激素诱导人乳头瘤病毒16 E6/E7永生化前列腺上皮细胞系分化。

Androgen induces differentiation of a human papillomavirus 16 E6/E7 immortalized prostate epithelial cell line.

作者信息

Ling M T, Chan K W, Choo C K

机构信息

Department of Pathology, The University of Hong Kong, Hong Kong.

出版信息

J Endocrinol. 2001 Jul;170(1):287-96. doi: 10.1677/joe.0.1700287.

Abstract

Androgen signaling is crucial for the growth and development, as well as for tumorigenesis of the prostate. However, many of the prostate epithelial cell lines developed previously, either normal or tumorigenic, do not express androgen receptor (AR) or respond to androgen. In order to advance our understanding on how androgen signaling regulates the growth and the differentiation status, and affects tumorigenicity of the epithelial cell, we performed experiments on HPr-1, a prostate cell line recently immortalized from normal human prostate epithelial cells. In the present study, AR was stably transfected into HPr-1 cells by replication-defective retrovirus. Treatment of HPr-1AR cells with androgen resulted in cell differentiation and growth retardation accompanied with up-regulation of cytokeratins K8 and K18, prostate specific antigen, p21 and p27, and down-regulation of c-myc, bcl-2 and telomerase activity. Our results suggest that androgen promotes the process of differentiation in a human papillomavirus 16 E6/E7 immortalized prostate epithelial cell line which may reflect the normal effects of androgen on prostate cells.

摘要

雄激素信号传导对于前列腺的生长发育以及肿瘤发生至关重要。然而,先前建立的许多前列腺上皮细胞系,无论是正常的还是致瘤性的,都不表达雄激素受体(AR)或对雄激素无反应。为了加深我们对雄激素信号传导如何调节上皮细胞的生长和分化状态以及影响其致瘤性的理解,我们对HPr-1进行了实验,HPr-1是一种最近从正常人前列腺上皮细胞永生化而来的前列腺细胞系。在本研究中,通过复制缺陷型逆转录病毒将AR稳定转染到HPr-1细胞中。用雄激素处理HPr-1AR细胞导致细胞分化和生长迟缓,同时细胞角蛋白K8和K18、前列腺特异性抗原、p21和p27上调,c-myc、bcl-2和端粒酶活性下调。我们的结果表明,雄激素促进人乳头瘤病毒16 E6/E7永生化前列腺上皮细胞系中的分化过程,这可能反映了雄激素对前列腺细胞的正常作用。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验