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雌激素和孕激素轴在肿瘤干性中的作用:阐明分子机制及临床意义

Involvement of the Estrogen and Progesterone Axis in Cancer Stemness: Elucidating Molecular Mechanisms and Clinical Significance.

作者信息

Chen Bi, Ye Peng, Chen Yeh, Liu Tong, Cha Jong-Ho, Yan Xiuwen, Yang Wen-Hao

机构信息

Affiliated Cancer Hospital and Institute of Guangzhou Medical University, Guangzhou, China.

Institute of New Drug Development, China Medical University, Taichung, Taiwan.

出版信息

Front Oncol. 2020 Sep 4;10:1657. doi: 10.3389/fonc.2020.01657. eCollection 2020.

DOI:10.3389/fonc.2020.01657
PMID:33014829
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7498570/
Abstract

Estrogen and progesterone regulate the growth and development of human tissues, including the reproductive system and breasts, through estrogen and progesterone receptors, respectively. These receptors are also important indicators for the clinical prognosis of breast cancer and various reproductive cancers. Many studies have reported that cancer stem cells (CSCs) play a key role in tumor initiation, progression, metastasis, and recurrence. Although the role of estrogen and progesterone in human organs and various cancers has been studied, the molecular mechanisms underlying the action of these hormones on CSCs remain unclear. Therefore, further elucidation of the effects of estrogen and progesterone on CSCs should provide a new direction for developing pertinent therapies. In this review, we summarize the current knowledge on the estrogen and progesterone axis involved in cancer stemness and discuss potential therapeutic strategies to inhibit CSCs by targeting relevant pathways.

摘要

雌激素和孕激素分别通过雌激素受体和孕激素受体调节人体组织(包括生殖系统和乳房)的生长和发育。这些受体也是乳腺癌和各种生殖系统癌症临床预后的重要指标。许多研究报告称,癌症干细胞(CSCs)在肿瘤的起始、进展、转移和复发中起关键作用。尽管雌激素和孕激素在人体器官及各种癌症中的作用已得到研究,但这些激素作用于癌症干细胞的分子机制仍不清楚。因此,进一步阐明雌激素和孕激素对癌症干细胞的影响应为开发相关治疗方法提供新方向。在本综述中,我们总结了目前关于参与癌症干性的雌激素和孕激素轴的知识,并讨论了通过靶向相关途径抑制癌症干细胞的潜在治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3261/7498570/cbde7e126eeb/fonc-10-01657-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3261/7498570/0192cc0e111b/fonc-10-01657-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3261/7498570/cbde7e126eeb/fonc-10-01657-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3261/7498570/0192cc0e111b/fonc-10-01657-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3261/7498570/cbde7e126eeb/fonc-10-01657-g0002.jpg

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Cell Commun Signal. 2020 Jun 5;18(1):84. doi: 10.1186/s12964-020-00563-4.
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The activation of GPER inhibits cells proliferation, invasion and EMT of triple-negative breast cancer via CD151/miR-199a-3p bio-axis.GPER的激活通过CD151/miR-199a-3p生物轴抑制三阴性乳腺癌细胞的增殖、侵袭和上皮-间质转化。
Am J Transl Res. 2020 Jan 15;12(1):32-44. eCollection 2020.
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ERα36 as a Potential Therapeutic Target for Tamoxifen-Resistant Breast Cancer Cell Line Through EGFR/ERK Signaling Pathway.
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