Targeting Cellular Trafficking of Fibroblast Growth Factor Receptors as a Strategy for Selective Cancer Treatment

Natalia Porębska1, Marta Latko2, Marika Kucińska3

  • 1Department of Protein Engineering, Faculty of Biotechnology, University of Wrocław, Joliot-Curie 14a, 50-383 Wroclaw, Poland. natalia.porebska2@uwr.edu.pl.

Insights

Fibroblast growth factor receptors (FGFRs) regulate cell processes and are implicated in cancer. Targeting FGFRs

Area of Science:

  • Cell Biology
  • Molecular Oncology
  • Cancer Therapeutics

Background:

  • Fibroblast growth factor receptors (FGFRs) and their ligands (FGFs) are crucial for cellular functions, including differentiation, division, motility, and apoptosis.
  • Aberrant FGFR signaling, driven by overproduction, mutations, or fusion proteins, is frequently observed in various cancers, promoting tumor growth and survival.

Purpose of the Study:

  • To review the current understanding of FGFRs' role in oncogenesis, focusing on their intracellular trafficking and implications for cancer.
  • To explore how FGFRs' subcellular localization (cell surface, nucleus, mitochondria) influences cancer progression and presents therapeutic opportunities.

Main Methods:

  • Review of existing literature on FGFRs' cellular trafficking mechanisms, including internalization, nuclear translocation, and mitochondrial targeting.
  • Analysis of the role of intracellular FGFR pools in cancer cell survival and expansion.
  • Examination of therapeutic strategies targeting FGFRs' subcellular localization.

Main Results:

  • Intracellular FGFRs contribute to cancer cell survival and proliferation through distinct mechanisms.
  • FGFRs' trafficking to the nucleus and mitochondria plays a significant role in cancer invasion and progression.
  • Endocytosis of FGFRs offers a pathway for targeted drug delivery into cancer cells.

Conclusions:

  • The subcellular sorting and trafficking of FGFRs represent a promising target for novel anti-cancer therapies.
  • Inhibiting FGFR nuclear and mitochondrial translocation can impede cancer invasion.
  • Hijacking FGFR endocytosis enables selective drug delivery for cancer treatment.

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