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Related Experiment Video

Updated: Aug 22, 2025

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EID3 Promotes Glioma Cell Proliferation and Survival by Inactivating AMPKα1.

Yaoxian Xiang1,2,3, Lei Zhu4, Zijian He5

  • 1Department of Hand Surgery, Huashan Hospital, Fudan University, Shanghai, China.

Journal of Korean Neurosurgical Society
|November 7, 2022
PubMed
Summary

EP300-interacting inhibitor of differentiation 3 (EID3) drives glioma growth by suppressing AMP-activated protein kinase α1 (AMPKα1). Inhibiting EID3 may offer a new glioma treatment strategy.

Keywords:
AMP activated protein kinase α1EP300-interacting inhibitor of differentiationGlioma

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • EP300-interacting inhibitor of differentiation 3 (EID3) is implicated in colorectal cancer.
  • The role of EID3 in glioma pathogenesis was previously unknown.

Purpose of the Study:

  • To investigate the function of EID3 in human glioma.
  • To identify EID3 as a potential therapeutic target for glioma.

Main Methods:

  • Analysis of EID3 expression in patient-derived glioma tissues and cell lines.
  • In vitro assays assessing cell proliferation, viability, and apoptosis.
  • In vivo studies using xenograft models in SCID mice.
  • Real-time PCR, Western blot, and MTT assays were employed.

Main Results:

  • EID3 is overexpressed in glioma tissues and cells compared to normal brain tissues.
  • EID3 knockdown suppressed glioma cell proliferation, invasion, viability, and induced apoptosis.
  • EID3 knockdown inhibited tumor growth in vivo.
  • AMP-activated protein kinase α1 (AMPKα1) was identified as a downstream mediator of EID3's oncogenic effects.

Conclusions:

  • EID3 promotes glioma cell proliferation and survival by inhibiting AMPKα1.
  • Targeting EID3 presents a potential therapeutic strategy for glioma treatment.