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TRIM59 Promotes Gliomagenesis by Inhibiting TC45 Dephosphorylation of STAT3

Youzhou Sang1, Yanxin Li2, Lina Song1

  • 1State Key Laboratory of Oncogenes and Related Genes, Renji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.

Cancer Research
|February 2, 2018
PubMed

Insights

Tripartite motif-containing protein 59 (TRIM59) is a novel downstream effector of epidermal growth factor receptor (EGFR) signaling in glioblastoma. Targeting TRIM59 may offer a new therapeutic strategy for glioblastoma patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Signaling

Background:

  • Aberrant epidermal growth factor receptor (EGFR) signaling drives glioblastoma (GBM) pathogenesis.
  • Downstream effectors sustaining EGFR oncogenic signaling in GBM are not fully understood.

Purpose of the Study:

  • To identify novel downstream effectors of EGFR signaling in GBM.
  • To investigate the role of tripartite motif-containing protein 59 (TRIM59) in GBM tumorigenesis.

Main Methods:

  • Investigated TRIM59 as a downstream effector of EGFR signaling.
  • Examined the regulation of STAT3 activation by TRIM59.
  • Assessed the impact of TRIM59 silencing on GBM cell proliferation, migration, and tumor formation.
  • Correlated EGFR activation, TRIM59 expression, and STAT3 phosphorylation with GBM patient prognoses.

Main Results:

  • EGFR signaling upregulates TRIM59 via SOX9, enhancing TRIM59 interaction with nuclear STAT3.
  • TRIM59 prevents STAT3 dephosphorylation by TC45, maintaining STAT3 transcriptional activity.
  • TRIM59 silencing inhibits GBM cell proliferation, migration, and orthotopic xenograft formation.
  • GBM patient samples show a link between EGFR activation, TRIM59 expression, STAT3 phosphorylation, and poor prognosis.

Conclusions:

  • TRIM59 is a novel downstream effector of EGFR/STAT3 signaling in GBM.
  • TRIM59 plays a critical role in GBM cell proliferation, migration, and tumorigenesis.
  • TRIM59 represents a potential therapeutic target for EGFR-activated GBM.

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