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SOX4 inhibits GBM cell growth and induces G0/G1 cell cycle arrest through Akt-p53 axis

Jing Zhang1,2, Huawei Jiang3,4, Jiaofang Shao5

  • 1Cancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education), Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang Province, P R China. jingzh1985@gmail.com.

BMC Neurology
|November 5, 2014
PubMed
Abstract

Insights

SOX4 acts as a tumor suppressor in glioblastoma multiforme (GBM). High SOX4 expression correlates with better prognosis by inhibiting GBM cell growth and inducing cell cycle arrest.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • SOX4 is a crucial transcription factor for vertebrate development.
  • SOX4 overexpression is observed in various cancers, including glioblastoma multiforme (GBM).
  • The precise role and mechanisms of SOX4 in GBM remain largely uncharacterized.

Purpose of the Study:

  • To investigate the functional role of SOX4 in glioblastoma multiforme.
  • To elucidate the underlying molecular mechanisms of SOX4 action in GBM.

Main Methods:

  • Kaplan-Meier survival analysis of primary GBM samples based on SOX4 expression.
  • Generation of SOX4 gain/loss models in GBM cells using the Cre/lox P system.
  • Microarray analysis to identify SOX4-regulated networks and pathways in GBM cells.

Main Results:

  • High SOX4 expression is significantly associated with favorable prognosis in primary GBM.
  • SOX4 suppresses the proliferation of GBM cell lines (LN229, A172G, U87MG).
  • SOX4 exerts its effects through p53-p21 activation, reduced AKT1 phosphorylation, and modulation of Wnt/β-catenin and TGF-β signaling pathways.

Conclusions:

  • SOX4 functions as a tumor suppressor in glioblastoma.
  • SOX4 induces cell cycle arrest and inhibits GBM cell growth.
  • SOX4's tumor-suppressive role involves p53-p21 signaling and affects key cancer-related pathways.

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