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Updated: Jan 31, 2026

A Mouse Model to Investigate the Role of Cancer-Associated Fibroblasts in Tumor Growth
Published on: December 22, 2020
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.
Abstract:
Fibroblast growth factor receptors (FGFRs) in response to fibroblast growth factors (FGFs) transmit signals across the cell membrane, regulating important cellular processes, like differentiation, division, motility, and death. The aberrant activity of FGFRs is often observed in various diseases, especially in cancer. The uncontrolled FGFRs' function may result from their overproduction, activating mutations, or generation of FGFRs' fusion proteins. Besides their typical subcellular localization on the cell surface, FGFRs are often found inside the cells, in the nucleus and mitochondria. The intracellular pool of FGFRs utilizes different mechanisms to facilitate cancer cell survival and expansion. In this review, we summarize the current stage of knowledge about the role of FGFRs in oncogenic processes. We focused on the mechanisms of FGFRs' cellular trafficking-internalization, nuclear translocation, and mitochondrial targeting, as well as their role in carcinogenesis. The subcellular sorting of FGFRs constitutes an attractive target for anti-cancer therapies. The blocking of FGFRs' nuclear and mitochondrial translocation can lead to the inhibition of cancer invasion. Moreover, the endocytosis of FGFRs can serve as a tool for the efficient and highly selective delivery of drugs into cancer cells overproducing these receptors. Here, we provide up to date examples how the cellular sorting of FGFRs can be hijacked for selective cancer treatment.
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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