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雌激素受体配体对二氢睾酮诱导的内皮细胞和前列腺癌细胞增殖的调节作用的差异。

Differential effects of estrogen receptor ligands on regulation of dihydrotestosterone-induced cell proliferation in endothelial and prostate cancer cells.

机构信息

The Third Xiangya Hospital, Central South University, Changsha, People's Republic of China.

出版信息

Int J Oncol. 2013 Jan;42(1):327-37. doi: 10.3892/ijo.2012.1689. Epub 2012 Nov 6.

DOI:10.3892/ijo.2012.1689
PMID:23135751
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3583656/
Abstract

Androgen deprivation therapy of prostate cancer with estrogens shows significant cardiovascular side-effects. To develop effective prostate cancer therapeutic agent(s) with minimal cardiovascular side-effects, we compared the effects of various estrogen receptor (ER) ligands on the modulation of dihydrotestosterone (DHT) actions in LAPC-4 and LNCaP prostate cancer cells and human aortic endothelial cells (HAECs). DHT stimulated the proliferation of HAEC, LAPC-4 and LNCaP cells and induced PSA mRNA expression in LAPC-4 cells. These DHT actions were differentially modulated by ER ligands in a cell-dependent manner. In LAPC-4 cells, knockdown of ERβ expression partially eliminated the βE2 inhibition of DHT-induced LAPC-4 cell proliferation, and a parallel change was observed between ER ligand modulation of DHT-induced cell proliferation and cyclin A expression. The obtained data suggest that it is feasible to develop effective agent(s) for prostate cancer therapy with minimal cardiovascular side-effects and 17α-estradiol and genistein are such potential agents.

摘要

雌激素的前列腺癌去势治疗显示出显著的心血管副作用。为了开发具有最小心血管副作用的有效前列腺癌治疗剂，我们比较了各种雌激素受体 (ER) 配体对前列腺癌细胞（LAPC-4 和 LNCaP）和人主动脉内皮细胞 (HAEC) 中双氢睾酮 (DHT) 作用的调节作用。DHT 刺激 HAEC、LAPC-4 和 LNCaP 细胞的增殖，并诱导 LAPC-4 细胞中 PSA mRNA 的表达。这些 DHT 作用在细胞依赖性方式下被 ER 配体以不同的方式调节。在 LAPC-4 细胞中，ERβ表达的敲低部分消除了βE2 对 DHT 诱导的 LAPC-4 细胞增殖的抑制作用，并且在 DHT 诱导的细胞增殖和细胞周期蛋白 A 表达的 ER 配体调节之间观察到平行变化。所得数据表明，开发具有最小心血管副作用的有效前列腺癌治疗剂是可行的，17α-雌二醇和金雀异黄素就是这样的潜在药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6476/3583656/43ead7bfd128/IJO-42-01-0327-g08.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6476/3583656/8909a409c878/IJO-42-01-0327-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6476/3583656/f70cdd65cc40/IJO-42-01-0327-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6476/3583656/cdb5db2847d9/IJO-42-01-0327-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6476/3583656/01086f2ed610/IJO-42-01-0327-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6476/3583656/a730f2f16994/IJO-42-01-0327-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6476/3583656/ca85c9c26087/IJO-42-01-0327-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6476/3583656/b6b6206a3a31/IJO-42-01-0327-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6476/3583656/43ead7bfd128/IJO-42-01-0327-g08.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6476/3583656/8909a409c878/IJO-42-01-0327-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6476/3583656/f70cdd65cc40/IJO-42-01-0327-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6476/3583656/cdb5db2847d9/IJO-42-01-0327-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6476/3583656/01086f2ed610/IJO-42-01-0327-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6476/3583656/a730f2f16994/IJO-42-01-0327-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6476/3583656/ca85c9c26087/IJO-42-01-0327-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6476/3583656/b6b6206a3a31/IJO-42-01-0327-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6476/3583656/43ead7bfd128/IJO-42-01-0327-g08.jpg

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本文引用的文献

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Estrogen regulates tumor growth through a nonclassical pathway that includes the transcription factors ERβ and KLF5.
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