Literature DB >> 31460785

MiR-204 suppresses cell proliferation and promotes apoptosis in ovarian granulosa cells via targeting TPT1 in polycystic ovary syndrome.

Xueqin Sun1, Shan Su1, Guoxiang Zhang2, Hong Zhang1, Xiaohui Yu1.   

Abstract

MicroRNA (miR)-204 is known to be associated with several different diseases. Polycystic ovary syndrome (PCOS) has the highest incidence rate among the endocrine disorders in females between the ages of 18 and 44. We aimed to illustrate the miR-204 function in PCOS. MiR-204 expression levels in tissue and cell were examined through RT-qPCR. Colony formation assay and MTT assay were applied to detect the cell viability. Flow cytometry was employed to examine the apoptosis and cell cycle in cells. RNA binding protein immunoprecipitation assay and luciferase reporter assay were provided to demonstrate the direct interaction between translationally controlled tumor protein (TPT1) and miR-204. The expression of miR-204 was declined in KGN cells and ovarian cortex tissues of PCOS patients. MiR-204 enhanced the colony formation capacity and cell proliferation in KGN cells. Cell cycle and apoptosis were also influenced by miR-204. Since miR-204 has direct interaction with TPT1, TPT1 overexpression suppressed the miR-204-induced apoptosis and cell cycle alteration in KGN cells. MiR-204 inhibits the cell viability and induces apoptosis and cell cycle arrest by directly interacting with TPT1, indicating a role of miR-204 to be a potential target in the PCOS patients.

Entities:  

Keywords:  TPT1; cellules de la granulosa; miR-204; ovarian granulosa cells; polycystic ovary syndrome; syndrome des ovaires polykystiques

Mesh:

Substances:

Year:  2019        PMID: 31460785     DOI: 10.1139/bcb-2019-0019

Source DB:  PubMed          Journal:  Biochem Cell Biol        ISSN: 0829-8211            Impact factor:   3.626


  6 in total

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6.  CircASPH promotes KGN cells proliferation through miR-375/MAP2K6 axis in Polycystic Ovary Syndrome.

Authors:  Gengxiang Wu; Jing Xia; Zhe Yang; Yajie Chen; Wei Jiang; Tailang Yin; Jing Yang
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  6 in total

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