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Blocking the bFGF/STAT3 interaction through specific signaling pathways induces apoptosis in glioblastoma cells

Jingchao Wu1, Xuequan Feng, Biao Zhang

  • 1Department of Neurosurgery, Tianjin Huanhu Hospital, Tianjin, 300060, People's Republic of China.

Journal of Neuro-Oncology
|July 23, 2014
PubMed

Insights

Basic fibroblast growth factor (bFGF) activates signal transducer and activator of transcription 3 (STAT3) via JAK and PI3K/Akt pathways in glioblastoma. STAT3 inhibition promotes apoptosis and reduces tumor growth.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Basic fibroblast growth factor (bFGF) is linked to malignant brain tumors, but its precise role and interaction with signal transducer and activator of transcription 3 (STAT3) remain unclear.
  • Understanding the bFGF/STAT3 pathway is crucial for developing targeted glioblastoma therapies.

Purpose of the Study:

  • To elucidate the mechanisms by which bFGF crosstalks with STAT3 in glioblastoma (GBM) cells.
  • To investigate the impact of the bFGF/STAT3 pathway on GBM cell apoptosis and tumor growth.

Main Methods:

  • Utilized pathway inhibitors (JAK, PI3K/Akt, Src) in U251 and U87 glioblastoma cell lines.
  • Employed siRNA-mediated knockdown of STAT3 to assess its effect on bFGF levels and apoptosis.
  • Evaluated mitochondrial membrane potential in vitro and tumor growth in vivo.

Main Results:

  • bFGF activates STAT3 primarily through the JAK and PI3K/Akt signaling pathways.
  • STAT3 knockdown significantly reduced bFGF levels in U251 cells.
  • STAT3 inhibition led to increased pro-apoptotic gene expression, decreased anti-apoptotic gene expression, mitochondrial dysfunction, and impaired tumor growth.

Conclusions:

  • bFGF-induced STAT3 activation is mediated by JAK and PI3K/Akt pathways in glioblastoma.
  • Targeting the bFGF/STAT3 pathway, particularly STAT3, holds therapeutic potential for glioblastoma by promoting apoptosis and inhibiting tumor progression.

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