KLF4 overexpression facilitates proliferation and represses apoptosis of granulosa cells in polycystic ovary syndrome

被引:0
|
作者
Miao, Hui [1 ]
Miao, Congxiu [1 ]
Li, Na [1 ]
Han, Jing [1 ]
机构
[1] Changzhi Med Coll, Key Lab Reprod Engineer Shanxi Hlth Comm, Inst Reprod & Genet, Heping Hosp,Key Lab Reprod & Genet,Dept Reprod Gen, Changzhi 046000, Shanxi, Peoples R China
基金
中国国家自然科学基金;
关键词
Polycystic ovary syndrome; KLF4; RUNX2; Ovarian granulosa cells; Proliferation; TESTOSTERONE; EXPRESSION; WOMEN; RUNX2;
D O I
10.1007/s13273-023-00354-1
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
BackgroundPolycystic ovary syndrome (PCOS) is defined as a complex endocrinopathy greatly affecting reproductive-aged women. Kruppel-like factors (KLFs) are involved in female reproduction.ObjectivesOur study expounded the functions of KLF4 on proliferation and apoptosis of ovarian granulosa cells (GCs) in PCOS via regulating Runt-related transcription factor 2 (RUNX2).ResultsKLF4 and RUNX2 were under-expressed in testosterone (TTR)-induced KGN cell models. KLF4 overexpression facilitated KGN cell proliferation and suppressed KGN cell apoptosis. KLF4 bound to the RUNX2 promoter and increased RUNX2 expression level. Furthermore, RUNX2 suppression counteracted the functions of KLF4 overexpression on KGN cells.ConclusionKLF4 overexpression promoted RUNX2 expression by binding to the RUNX2 promoter, thereby further accelerating GC proliferation and repressing GC apoptosis in PCOS.
引用
收藏
页码:97 / 106
页数:10
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