Journal
REPRODUCTIVE SCIENCES
Volume 21, Issue 3, Pages 386-394Publisher
SAGE PUBLICATIONS INC
DOI: 10.1177/1933719113497281
Keywords
AR; endometrial cancer; cancer stem; progenitor cells; cisplatin resistance; side population cell
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Funding
- National Science Council [NSC100-2314-B-039041, NSC100-2320-B-039-036]
- China Medical University Hospital, Taiwan [DMR101-070]
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Endometrial cancer (EMC) is a sex steroid hormone-related female malignancy. Androgen and androgen receptor (androgen/AR) signals have been implicated in EMC progression. Cancer stem/progenitor cells (CSPCs) are suspected to link to chemoresistance in patients with EMC. In this study, we examined the androgen/AR roles in cisplatin resistance and CSPC population. We found AR expression increased naive EMC side population, CSPC population, cell migration, and epithelial-mesenchymal transition. Meanwhile, it decreased cisplatin cytotoxic effect on EMC cells. Collaterally, endogenous AR expressions in EMC cells were upregulated in the cisplatin-resisting state. Moreover, AR expression could further enhance CD133 expression, CSPC-related markers, and drug-resistance gene messenger RNA expression in EMC cells. Finally, the AR-associated gene expression might go through indirect regulation. This is the first report revealing AR function on EMC cells' CSPC and cisplatin resistance.
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