Journal
GYNECOLOGICAL ENDOCRINOLOGY
Volume 38, Issue 11, Pages 965-970Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1080/09513590.2022.2123914
Keywords
Polycystic ovary syndrome; IL23; proliferation; apoptosis; cell cycle; AR
Funding
- National Key Research and Development Program of China [2018YFC1003202, 2016YFC1000604]
- Taishan scholar Engineering [ts201712103]
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This study found that IL23 suppressed the proliferation of GCs and promoted apoptosis. It was also discovered that this process was mediated by AR signaling. These findings provide new evidence for the abnormal proliferation and apoptosis of GCs in PCOS.
Background: Polycystic ovary syndrome (PCOS) is associated with chronic low-grade inflammation. IL23 is a classic pro-inflammatory factor, which has been found that serum levels of IL23 were higher in patients with PCOS. However, the exact function of IL23 in regulating the pathogenesis of PCOS has not been elucidated. This study aimed to investigate the role of IL23 in the pathogenesis of PCOS and uncover the possible molecular mechanism. Methods: We investigated the role of IL23 in the proliferation, cell cycle progression and apoptosis of granulosa cells (GCs) using the human granulosa-like tumor cell line KGN. Results: IL23 suppressed the proliferation, arrested cell cycle progression, and increased apoptosis of KGN cells. We also found that IL23 decreases proliferation and promotes apoptosis in KGN cells is mediated by androgen receptor (AR) signaling. Conclusions: Our results demonstrated that IL23 suppressed cell proliferation and promoted apoptosis of KGN cells, which might provide new evidence for abnormal proliferation and apoptosis of GCs in PCOS.
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