Chao Nang Qing prescription promotes granulosa cell apoptosis and autophagy by targeting GATA3

Abstract

Objective Polycystic ovary syndrome (PCOS) is a common endocrine disease in women of reproductive age, with complex pathological symptoms and mechanisms. This study explored the mechanism of action of Chao Nang Qing prescription (CNQP) in PCOS. Methods CNQP-medicated serum was prepared for culturing KGN granulosa cells. GATA3 knockdown, MYCT1 overexpression, and MYCT1 knockdown vectors were constructed to transfect KGN cells. Cell proliferation and apoptosis, as well as the expression of autophagy-related LC3-II/I, Beclin-1, and p62, were analyzed. ChIP was used to detect the binding of GATA3 and the MYCT1 promoter, and dual-luciferase reporter assay was used to analyze the influence of GATA3 on MYCT1 promoter activity. Results CNQP treatment reduced proliferation, increased apoptosis, elevated LC3-II/I, Beclin-1, GATA3, and MYCT1 expression, and decreased p62 expression in KGN cells. GATA3 bound to the MYCT1 promoter to promote MYCT1 expression. MYCT1 overexpression impeded proliferation and stimulated apoptosis and autophagy in KGN cells. Compared to CNQP treatment alone, GATA3 or MYCT1 knockdown before CNQP treatment promoted proliferation and reduced apoptosis and autophagy in KGN cells. Conclusion CNQP may modulate KGN cell activity by upregulating GATA3 and MYCT1 expression, thereby slowing down the progression of PCOS.