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J Cell Mol Med. 2018 Jan;22(1):46-56. doi: 10.1111/jcmm.13291. Epub 2017 Aug 7.

Short androgen receptor poly-glutamine-promoted endometrial cancer is associated with benzo[a]pyrene-mediated aryl hydrocarbon receptor activation.

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Graduate Institution of Clinical Medical Science, Graduate Institute of BioMedical Sciences, Department of Pharmacy, China Medical University, Taichung, Taiwan.
Sex Hormone Research Center, Department of Obstetrics and Gynecology, Department of Pathology, Research Center for Tumor Medical Science, China Medical University/Hospital, Taichung, Taiwan.
Department of OBs & GYN, BenQ Medical Center, Nanjing Medical University, Suzhou, Jiangsu Province, China.
Department of Nursing, Asia University, Taichung, Taiwan.
Department of OBs& GYN, Chia-Yi Chang-Gong Memorial Hospital, Chia-Yi, Taiwan.
Chung-Jen Jounior College of Nursing, Health Sciences and Management, ChiaYi, Taiwan.


The androgen receptor (AR) poly-glutamine polymorphism (AR-Q) was reported to play role in endometrial cancer (EMCA) development, yet controversial. Environmental factors interact with genetic variation have been reported in EMCA. Aerosol toxins, polycyclic aromatic hydrocarbon benzo[a]pyrene (BaP), are EMCA facilitators. This report examined the interplay between AR-Qs and BaP in EMCA. During analysing patient AR-Q polymorphism and Aryl hydrocarbon Receptor (AhR) expressions, we found overall survival (OS) benefit is ascending with AR-Q lengths (5-year OS of 61.3% in Q length <20 and 88% in Q length >23). And AhR is higher expressed in short AR-Q tumour compared to that in long AR-Q patient. In vitro study found androgen-response element (ARE) activity descends with AR-Qs length (Q13 > Q25 > Q35), whereas BaP suppresses ARE activities in EMCA cells. Furthermore, AR-Q13 (but not AR-Q25, or -35) enhances BaP-induced dioxin-responsive element (DRE) activity. Lastly, AR-Q13 exerts higher colony-forming capacity than other AR-Qs, and knock-down AhR abolished AR-Q13-mediated colony numbers. This study demonstrated a possible interaction of gene (AR-Q polymorphism) and environmental toxins (e.g. BaP) to affect cancer progression. A large-scale epidemiology and public health survey on the interaction of environmental toxin and AR poly-Q in EMCA is suggested.


AR ; AhR; BaP; endometrial cancer; poly-Q polymorphism

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