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Updated: Jun 29, 2025

Isolation of Human Endometrial Stromal Cells for In Vitro Decidualization
14:55

Isolation of Human Endometrial Stromal Cells for In Vitro Decidualization

Published on: September 1, 2018

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KAT2A changes the function of endometrial stromal cells via regulating the succinylation of ENO1

Kangkang Zeng1, Hao Yin1

  • 1Department of Obstetrics and Gynecology, Taihe Hospital, Hubei University of Medicine, 32 Renmin South Road, Maojian District, Shiyan 442000, Hubei, China.

Open Life Sciences
|April 8, 2024
PubMed

Insights

Endometriosis progression is linked to KAT2A-mediated succinylation of ENO1. This study reveals KAT2A promotes malignant behavior in endometrial stromal cells, offering potential therapeutic targets for endometriosis.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Gynecology

Background:

  • Endometriosis affects many women globally, with pathogenesis research ongoing.
  • The role of succinylation genes in endometriosis remains unclear.
  • Identifying key molecular targets is crucial for understanding endometriosis development.

Purpose of the Study:

  • To investigate the role of succinylation genes, specifically KAT2A and ENO1, in endometriosis.
  • To determine the association between KAT2A and ENO1 in endometrial stromal cells (ESCs).
  • To elucidate the mechanism by which KAT2A influences endometriosis progression.

Main Methods:

  • Gene and protein expression analysis using qRT-PCR and Western blot.
  • Assessment of ESCs proliferation, apoptosis, migration, and invasion via CCK-8, Transwell, and flow cytometry assays.
  • Investigation of KAT2A and ENO1 interaction using Co-immunoprecipitation (CoIP) and immunofluorescence.

Main Results:

  • KAT2A expression was significantly higher in ectopic endometrium (EC) compared to control tissues.
  • KAT2A silencing reduced ESCs proliferation, migration, and invasion while increasing apoptosis.
  • KAT2A overexpression upregulated ENO1 expression and its succinylation, with KAT2A positively binding to ENO1.

Conclusions:

  • KAT2A plays a critical role in promoting malignant behaviors of ESCs in endometriosis.
  • Succinylation of ENO1 mediated by KAT2A is a key mechanism driving endometriosis progression.
  • Targeting the KAT2A-ENO1 pathway may offer a novel therapeutic strategy for endometriosis.
Keywords:
ENO1KAT2Aembryonic stem cellsendometriosis

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