细胞凋亡
白细胞介素23
多囊卵巢
癌症研究
细胞生物学
信号转导
细胞生长
炎症
内分泌学
生物
白细胞介素17
免疫学
胰岛素抵抗
糖尿病
遗传学
生物化学
作者
Wenqi Wang,Jing Hao,Yuhua Shi
标识
DOI:10.1080/09513590.2022.2123914
摘要
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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