Cholinergic signaling via muscarinic M1 receptor confers resistance to docetaxel in prostate cancer

被引：5

作者：

Wang, Jing ^{[1
]}

Wei, Jing ^{[1
]}

Pu, Tianjie ^{[1
]}

Zeng, Alan ^{[2
]}

Karthikeyan, Varsha ^{[3
,4
]}

Bechtold, Baron ^{[1
]}

Vo, Karen ^{[1
,3
]}

Chen, Jingrui ^{[1
]}

Lin, Tzu-Ping ^{[5
,6
,7
]}

Chang, Amy P. ^{[8
]}

Corey, Eva ^{[9
]}

Puhr, Martin ^{[10
]}

Klocker, Helmut ^{[10
]}

Culig, Zoran ^{[10
]}

Bland, Tyler ^{[1
,11
]}

Wu, Boyang Jason ^{[1
]}

机构：

[1] Washington State Univ, Coll Pharm & Pharmaceut Sci, Dept Pharmaceut Sci, Spokane, WA 99202 USA

[2] Univ Washington, Undergraduate Programs, Seattle, WA USA

[3] Washington State Univ, Coll Pharm & Pharmaceut Sci, Summer Undergraduate Res Fellowship Program, Spokane, WA USA

[4] Oregon State Univ, Sch Life Sci, Dept Integrat Biol, Corvallis, OR USA

[5] Taipei Vet Gen Hosp, Dept Urol, Taipei, Taiwan

[6] Natl Yang Ming Chiao Tung Univ, Sch Med, Dept Urol, Taipei, Taiwan

[7] Natl Yang Ming Chiao Tung Univ, Shu Tien Urol Res, Taipei, Taiwan

[8] Natl Yang Ming Chiao Tung Univ, Inst Microbiol & Immunol, Taipei, Taiwan

[9] Univ Washington, Dept Urol, Seattle, WA USA

[10] Med Univ Innsbruck, Dept Urol, Div Expt Urol, Innsbruck, Austria

[11] Univ Idaho, WWAMI Med Educ Program, Moscow, ID 83844 USA

来源：

CELL REPORTS MEDICINE | 2024年 / 5卷 / 02期

关键词：

MONOAMINE-OXIDASE; GENE-EXPRESSION; PROTEIN; ACTIVATION; CELLS; LANDSCAPE; EVOLUTION; GROWTH; MET;

D O I：

10.1016/j.xcrm.2023.101388

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Docetaxel is the most commonly used chemotherapy for advanced prostate cancer (PC), including castration -resistant disease (CRPC), but the eventual development of docetaxel resistance constitutes a major clinical challenge. Here, we demonstrate activation of the cholinergic muscarinic M1 receptor (CHRM1) in CRPC cells upon acquiring resistance to docetaxel, which is manifested in tumor tissues from PC patients post- vs. pre-docetaxel. Genetic and pharmacological inactivation of CHRM1 restores the efficacy of docetaxel in resistant cells. Mechanistically, CHRM1, via its first and third extracellular loops, interacts with the SEMA domain of cMET and forms a heteroreceptor complex with cMET, stimulating a downstream mitogen-activated protein polykinase program to confer docetaxel resistance. Dicyclomine, a clinically available CHRM1-selective antagonist, reverts resistance and restricts the growth of multiple docetaxel-resistant CRPC cell lines and patient -derived xenografts. Our study reveals a CHRM1-dictated mechanism for docetaxel resistance and identifies a CHRM1-targeted combinatorial strategy for overcoming docetaxel resistance in PC.

引用

页数：24

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