Related Experiment Video

Updated: Sep 21, 2025

Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter
11:32

Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter

Published on: March 27, 2020

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Transcription factor SNAI2 exerts pro-tumorigenic effects on glioma stem cells via PHLPP2-mediated Akt pathway

Lilei Peng1,2,3,4, Jie Fu5, Yitian Chen6

  • 1Department of Neurosurgery, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, PR China. lilei.peng@swmu.edu.cn.

Cell Death & Disease
|June 2, 2022
PubMed

Insights

Snail family transcriptional repressor 2 (SNAI2) promotes glioma stem cell proliferation by downregulating PHLPP2, activating the Akt pathway. This SNAI2-PHLPP2 interaction is a potential therapeutic target for glioma.

Area of Science:

  • Neuro-oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Glioma is a primary brain tumor with poor prognosis.
  • Glioma stem cells (GSCs) drive tumor growth and recurrence.
  • The role of SNAI2 in GSC proliferation requires further elucidation.

Purpose of the Study:

  • Investigate the effect of SNAI2 on GSC proliferation.
  • Elucidate the molecular mechanism of SNAI2 in glioma development.
  • Determine the relationship between SNAI2 and PHLPP2 in GSCs.

Main Methods:

  • Bioinformatics analysis and RT-qPCR for SNAI2 expression.
  • Loss- and gain-of-function assays for SNAI2 and PHLPP2.
  • Chromatin immunoprecipitation and Akt pathway analysis.
  • In vivo xenograft mouse model for glioma growth.

Main Results:

  • SNAI2 is highly expressed in glioma tissues and GSCs, inversely correlating with patient survival.
  • SNAI2 promotes GSC proliferation, while PHLPP2 inhibits it.
  • SNAI2 directly represses PHLPP2 transcription, leading to Akt pathway activation.
  • SNAI2 promotes glioma growth in vivo.

Conclusions:

  • SNAI2 promotes GSC proliferation and glioma growth by downregulating PHLPP2 and activating the Akt pathway.
  • Targeting the SNAI2-PHLPP2 axis may offer a therapeutic strategy for glioma.

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