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Updated: May 4, 2026

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
Published on: October 27, 2020
TGF-beta in CAF-mediated tumor growth and metastasis
A Calon1, D V F Tauriello1, E Batlle2
1Oncology Department, Institute for Research in Biomedicine, 08028 Barcelona, Spain.
Abstract:
TGF-beta signaling is one of the major pathways controlling cell and tissue behavior not only in homeostasis but also in disease. During tumorigenesis TGF-beta orchestrated processes are key due to its dual role as tumor suppressor and tumor promoter. Important functions of this pathway have been described in a context-dependent manner both in epithelial cancer cells and in the tumor microenvironment during tumor progression. Carcinoma-associated fibroblasts (CAFs) are one of the most abundant stromal cell types in virtually all solid tumors. CAFs favor malignant progression by providing cancer cells with proliferative, migratory, survival and invasive capacities. A complex network of signaling pathways underlying their tumor-promoting properties is beginning to take shape. In this review, we examine current evidence on the emerging mechanisms involving TGF-beta in CAF-mediated cancer progression, and discuss their potential as therapeutic targets.
Insights
Transforming growth factor-beta (TGF-beta) signaling plays a dual role in cancer. This review explores how TGF-beta in carcinoma-associated fibroblasts promotes tumor progression and identifies potential therapeutic targets.
Area of Science:
- Oncology
- Cell Biology
- Cancer Research
Background:
- Transforming growth factor-beta (TGF-beta) signaling is crucial for cell and tissue regulation in homeostasis and disease.
- TGF-beta exhibits a dual role in tumorigenesis, acting as both a tumor suppressor and promoter.
- Carcinoma-associated fibroblasts (CAFs) are abundant stromal cells that enhance malignant progression.
Purpose of the Study:
- To review emerging mechanisms of TGF-beta involvement in CAF-mediated cancer progression.
- To discuss the therapeutic potential of targeting TGF-beta signaling in CAFs.
Main Methods:
- Literature review of current evidence on TGF-beta signaling in cancer.
- Analysis of CAF functions and their interaction with cancer cells.
- Examination of signaling pathways involved in CAF-driven tumor promotion.
Main Results:
- TGF-beta signaling in CAFs contributes to cancer cell proliferation, migration, survival, and invasion.
- CAFs, influenced by TGF-beta, create a tumor-promoting microenvironment.
- Complex signaling networks mediate the tumor-promoting properties of CAFs.
Conclusions:
- TGF-beta signaling is a key driver of CAF-mediated tumor progression.
- Targeting TGF-beta pathways within CAFs represents a promising therapeutic strategy for cancer treatment.
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