Azurocidin is associated with dienogest-resistance in ovarian endometriotic cysts

Momoe Watanabe, Yoichi Kobayashi, Manami Ishida, Atsushi Tajima, Shinji Tanigaki, Tohru Morisada
In: Research Square · 2024 · doi:10.21203/rs.3.rs-3991408/v1 · W4392516059
preprint OA: green CC0
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⚙ AI-generated summary by claude@2026-06+body, 2026-06-07 ⓘ

Azurocidin suppresses dienogest's action on IL-6 and IL-8 in endometriotic cells by increasing estrogen receptor expression, suggesting it contributes to dienogest resistance.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

This preprint investigated how the inflammatory mediator azurocidin influences dienogest (DNG) responsiveness in ovarian endometriotic cysts using the human immortalized endometriotic epithelial Emosis-CC/TERT1 cell line. In the study, DNG inhibited IL-6 and IL-8 production, but this suppression was reduced when azurocidin was present; azurocidin itself increased IL-6 and IL-8–associated signaling and elevated estrogen receptor (ER) mRNA expression, with increased cell proliferation after exposure to 17β-estradiol plus azurocidin. The authors report that azurocidin may inhibit DNG action by increasing estrogen sensitivity via ER upregulation, linking azurocidin to DNG resistance, while noting the limitation that these findings are derived from an in vitro immortalized cell model and the work is not peer reviewed. This paper is centrally about endometriosis—specifically ovarian endometriotic cysts and molecular mechanisms associated with dienogest resistance involving azurocidin and estrogen receptor signaling.

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