IL23 suppresses proliferation and promotes apoptosis of human granulosa-like tumor cell line KGN by targeting the androgen receptor signal pathway

Abstract

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.

摘要

背景

多囊卵巢综合征(PCOS)与慢性低度炎症有关。IL23是一种经典的促炎因子, 已发现PCOS患者血清IL23水平较高。然而, IL23在PCOS发病机制中的确切作用尚不清楚。本研究旨在探讨IL23在PCOS发病机制中的作用, 并揭示其可能的分子机制。

方法

研究IL23在人颗粒样肿瘤细胞系KGN的增殖、细胞周期进程和细胞凋亡中的作用。

结果

IL23抑制KGN细胞增殖, 阻止细胞周期进程, 促进细胞凋亡。我们还发现IL23通过雄激素受体(AR)信号通路发挥对KGN细胞的增殖抑制和凋亡促进作用。

结论

IL23抑制KGN细胞增殖, 促进KGN细胞凋亡, 为PCOS中GCs的异常增殖和凋亡提供了新的证据。

Keywords:

• Polycystic ovary syndrome
• IL23
• proliferation
• apoptosis
• cell cycle
• AR

关键词:

• 多囊卵巢综合征
• IL23
• 增殖
• 凋亡
• 细胞周期
• AR

Authors’ contributions

Yuhua Shi and Jing Hao conceived and designed this study. Wenqi Wang contributed to experiments, statistical analysis, interpretation of data, and manuscript draft. Yuhua Shi participated in the discussion and critically revised the manuscript. All authors read and approved the final manuscript.

Availability of data and materials

The datasets generated for this study are available on request to the corresponding author.

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

This work was supported by the National Key Research and Development Program of China (2018YFC1003202, 2016YFC1000604), Special funds for Taishan scholar Engineering (ts201712103).