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Updated: Oct 2, 2025

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
Published on: October 27, 2020
Fibroblast growth factor receptor signalling dysregulation and targeting in breast cancer
Chiara Francavilla1,2, Ciara S O'Brien3,2
1Division of Molecular and Cellular Function, School of Biological Science, Faculty of Biology, Medicine and Health (FBMH), University of Manchester, Manchester M13 9PT, UK.
Abstract:
Fibroblast Growth Factor Receptor (FGFR) signalling plays a critical role in breast embryonal development, tissue homeostasis, tumorigenesis and metastasis. FGFR, its numerous FGF ligands and signalling partners are often dysregulated in breast cancer progression and are one of the causes of resistance to treatment in breast cancer. Furthermore, FGFR signalling on epithelial cells is affected by signals from the breast microenvironment, therefore increasing the possibility of breast developmental abnormalities or cancer progression. Increasing our understanding of the multi-layered roles of the complex family of FGFRs, their ligands FGFs and their regulatory partners may offer novel treatment strategies for breast cancer patients, as a single agent or rational co-target, which will be explored in depth in this review.
Insights
Fibroblast Growth Factor Receptor (FGFR) signaling is crucial in breast development and cancer. Understanding FGFR dysregulation offers new therapeutic targets for breast cancer treatment and resistance.
Area of Science:
- Oncology
- Developmental Biology
- Cell Signaling
Background:
- Fibroblast Growth Factor Receptor (FGFR) signaling is vital for normal breast development and tissue maintenance.
- Dysregulation of FGFRs and their ligands (FGFs) is implicated in breast cancer progression and treatment resistance.
- The breast microenvironment influences FGFR signaling, impacting development and cancer aggressiveness.
Purpose of the Study:
- To review the complex roles of FGFRs, FGF ligands, and regulatory partners in breast cancer.
- To explore the potential of targeting FGFR signaling for novel breast cancer therapies.
- To understand how microenvironmental signals modulate FGFR activity in breast epithelial cells.
Main Methods:
- Literature review of studies on FGFR signaling in breast biology and cancer.
- Analysis of genetic and molecular alterations in FGFR pathways in breast tumors.
- Examination of preclinical and clinical data on FGFR-targeted therapies.
Main Results:
- FGFR signaling pathways are frequently altered in various breast cancer subtypes.
- FGFRs contribute to tumor initiation, growth, metastasis, and resistance to endocrine and chemotherapy.
- Targeting FGFRs shows promise, but challenges related to specificity and resistance mechanisms exist.
Conclusions:
- A comprehensive understanding of FGFR signaling complexity is essential for developing effective breast cancer treatments.
- Targeting FGFRs, alone or in combination, represents a promising strategy for overcoming treatment resistance.
- Further research into FGFR regulation by the tumor microenvironment may reveal new therapeutic avenues.
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