Activation of Wnt/β-catenin signaling in a subpopulation of murine prostate luminal epithelial cells induces high grade prostate intraepithelial neoplasia.
Activation of Wnt/β-catenin signaling in a subpopulation of murine prostate luminal epithelial cells induces high grade prostate intraepithelial neoplasia.
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DOI：
10.1002/pros.22868
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发表时间：
2014-11
期刊：
影响因子：
2.8
通讯作者：
Williams, Bart O.
中科院分区：
文献类型：
--
作者：
Valkenburg, Kenneth C.;Yu, Xiuping;De Marzo, Angelo M.;Spiering, Tyler J.;Matusik, Robert J.;Williams, Bart O.
Wnt/β-catenin signaling is important for prostate development and cancer in humans. Activation of this pathway in differentiated luminal cells of mice induces high-grade prostate intraepithelial neoplasia (HGPIN). Though the cell of origin of prostate cancer has yet to be conclusively identified, a castration-resistant Nkx3.1-expressing cell (CARN) may act as a cell of origin for prostate cancer. To activate Wnt/β-catenin signaling in CARNs, we crossed mice carrying tamoxifen-inducible Nkx3.1-driven Cre to mice containing loxP sites in order to either conditionally knock out adenomatous polyposis coli (Apc) or constitutively activate β-catenin directly. We then castrated and hormonally regenerated these mice to target the CARN population. Loss of Apc in hormonally normal mice induced HGPIN; however, after one or more rounds of castration and hormonal regeneration, Apc-null CARNs disappeared. Alternatively, when β-catenin was constitutively activated under the same conditions, HGPIN was apparent. Activation of Wnt/β-catenin signaling via Apc deletion is sufficient to produce HGPIN in hormonally normal mice. Loss of Apc may destabilize the CARN population under regeneration conditions. When β-catenin is constitutively activated, HGPIN occurs in hormonally regenerated mice. A second genetic hit is likely required to cause progression to carcinoma and metastasis.
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DOI：
10.1126/science.1189992
发表时间：
2010-07-30
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Goldstein AS;Huang J;Guo C;Garraway IP;Witte ON
通讯作者：
Witte ON
影响因子：
2.5
作者：
Mehta, Vatsal;Abler, Lisa L.;Keil, Kimberly P.;Schmitz, Christopher T.;Joshi, Pinak S.;Vezina, Chad M.
通讯作者：
Vezina, Chad M.
影响因子：
4.8
作者：
Carayol, Nathalie;Wang, Cun-Yu
通讯作者：
Wang, Cun-Yu
TAZ 促进细胞增殖和上皮间质转化，并受 hippo 通路抑制
影响因子：
5.3
作者：
Lei, Qun-Ying;Zhang, Heng;Guan, Kun-Liang
通讯作者：
Guan, Kun-Liang
影响因子：
5.2
作者：
Chen, Yang;Li, Jie;Hu, Yanling
通讯作者：
Hu, Yanling