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Receptor Tyrosine Kinases: Principles and Functions in Glioma Invasion

Mitsutoshi Nakada1, Daisuke Kita2, Lei Teng3,4

  • 1Department of Neurosurgery, Division of Neuroscience, Graduate School of Medical Science, Kanazawa University, 13-1 Takara-machi, Kanazawa, Ishikawa, 920-8640, Japan. mnakada@med.kanazawa-u.ac.jp.

Advances in Experimental Medicine and Biology
|February 9, 2020
PubMed

Insights

Receptor tyrosine kinases (RTKs) are crucial for cell signaling and cancer development. This review highlights RTK roles in glioma invasion, suggesting RTKs as potential therapeutic targets for brain tumors.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • Protein tyrosine kinases (PTKs) regulate cellular functions through phosphorylation.
  • Receptor tyrosine kinases (RTKs) are cell surface PTKs activated by ligand binding.
  • PTKs are vital in normal cellular processes and implicated in cancer development.

Purpose of the Study:

  • To summarize recent findings on the role of RTKs in glioma pathobiology.
  • To focus on the contribution of RTKs to the invasive phenotype of gliomas.
  • To explore the potential of RTKs as therapeutic targets for glioma treatment.

Main Methods:

  • Literature review of recent studies on RTKs in glioma.
  • Analysis of the role of specific RTKs (e.g., EGFR, PDGFR, c-Met) in glioma invasion.
  • Synthesis of current understanding of RTK signaling in glioma progression.

Main Results:

  • RTKs play a significant role in regulating normal cellular functions.
  • Specific RTKs, including EGFR, PDGFR, c-Met, Tie, Axl, DDR1, and Eph, are heavily involved in glioma invasion.
  • Dysregulation of RTK pathways contributes to the aggressive, invasive nature of gliomas.

Conclusions:

  • RTKs are key regulators of glioma pathobiology, particularly invasion.
  • Targeting RTKs presents a promising therapeutic strategy for combating glioma.
  • Further research into RTK signaling pathways may yield novel glioma treatments.
Keywords:
AxlClinical trialCross-talkDDR1EGFREphGlioblastomaGliomaInvasionPDGFRTieTrkATyrosine kinase inhibitorTyrosine kinase receptorc-Met

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