期刊
AMERICAN JOURNAL OF PATHOLOGY
卷 183, 期 5, 页码 1679-1687出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.ajpath.2013.07.026
关键词
-
类别
资金
- University of Houston Small Grant Program
- University of Houston New Faculty Award
- NIH [CA141583, R01 CA-77530, U54 HD-0077495]
- Texas Emerging Technology Fund (Center for Nuclear Receptors and Cell Signaling)
Human papillomavirus is the main cause of cervical cancer, yet other nonviral cofactors are also required for the disease. The uterine cervix is a hormone-responsive tissue, and female hormones have been implicated in cervical carcinogenesis. A transgenic mouse model expressing human papillomavirus oncogenes E6 and/or E7 has proven useful to study a mechanism of hormone actions in the context of this common malignancy. Estrogen and estrogen receptor cc are required for the development of cervical cancer in this mouse model. Estrogen receptor a is known to up-regulate expression of the progesterone receptor, which, on activation by its Ligands, either promotes or inhibits carcinogenesis, depending on the tissue context. Here, we report that progesterone receptor inhibits cervical and vaginal epithelial cell proliferation in a Ligand-dependent manner. We also report that synthetic progestin medroxyprogesterone acetate promotes regression of cancers and precancerous Lesions in the female lower reproductive tracts (ie, cervix and vagina) in the human papillomavirus transgenic mouse model. Our results provide the first experimental evidence that supports the hypothesis that progesterone signaling is inhibitory for cervical carcinogenesis in vivo.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据