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Updated: Mar 22, 2026

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Control of glioblastoma tumorigenesis by feed-forward cytokine signaling

Arezu Jahani-Asl1,2,3,4,5, Hang Yin3,6,7,8, Vahab D Soleimani5,9

  • 1Department of Neurobiology, Harvard Medical School, Boston, Massachusetts, USA.

Nature Neuroscience
|April 26, 2016
PubMed

Insights

The cytokine receptor OSMR is a key co-receptor for EGFRvIII in glioblastoma. Targeting OSMR significantly suppressed tumor growth and improved survival in glioblastoma models.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Epidermal Growth Factor Receptor variant III (EGFRvIII) and Signal Transducer and Activator of Transcription 3 (STAT3) signaling pathways are crucial in glioblastoma (GBM) development.
  • Identifying novel molecular targets is essential for effective GBM treatment strategies.

Purpose of the Study:

  • To investigate the role of the cytokine receptor OSMR in EGFRvIII-driven glioblastoma.
  • To elucidate the interaction between OSMR, EGFRvIII, and STAT3 signaling in tumorigenesis.

Main Methods:

  • Identified OSMR as a direct STAT3 target gene in mouse astrocytes and human brain tumor stem cells (BTSCs).
  • Investigated the physical interaction between OSMR and EGFRvIII using co-immunoprecipitation assays.
  • Assessed the impact of OSMR depletion and EGFRvIII inhibition on signaling pathways and tumor growth in vitro and in vivo xenograft models.

Main Results:

  • OSMR acts as an essential co-receptor for EGFRvIII, forming a complex that is critical for EGFRvIII-STAT3 signaling.
  • Depletion of OSMR or inhibition of EGFRvIII phosphorylation disrupted this signaling axis.
  • OSMR knockdown significantly suppressed glioblastoma cell proliferation and tumor growth in vivo, prolonging mouse survival.

Conclusions:

  • OSMR is a critical regulator of glioblastoma tumor growth, functioning in a feed-forward loop with EGFRvIII and STAT3.
  • Targeting the OSMR-EGFRvIII interaction presents a potential therapeutic strategy for glioblastoma.

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