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Updated: Jun 22, 2025
Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
Published on: October 27, 2020
TGF-β signaling: critical nexus of fibrogenesis and cancer
Anna O Giarratana1, Conor M Prendergast2, Mary M Salvatore3
1Northwell Health - Peconic Bay Medical Center, 1 Heroes Way, Riverhead, NY, 11901, USA. agiarratana@northwell.edu.
Abstract:
The transforming growth factor-beta (TGF-β) signaling pathway is a vital regulator of cell proliferation, differentiation, apoptosis, and extracellular matrix production. It functions through canonical SMAD-mediated processes and noncanonical pathways involving MAPK cascades, PI3K/AKT, Rho-like GTPases, and NF-κB signaling. This intricate signaling system is finely tuned by interactions between canonical and noncanonical pathways and plays key roles in both physiologic and pathologic conditions including tissue homeostasis, fibrosis, and cancer progression. TGF-β signaling is known to have paradoxical actions. Under normal physiologic conditions, TGF-β signaling promotes cell quiescence and apoptosis, acting as a tumor suppressor. In contrast, in pathological states such as inflammation and cancer, it triggers processes that facilitate cancer progression and tissue remodeling, thus promoting tumor development and fibrosis. Here, we detail the role that TGF-β plays in cancer and fibrosis and highlight the potential for future theranostics targeting this pathway.
Insights
Transforming growth factor-beta (TGF-β) signaling regulates cell functions and tissue homeostasis. Its dual role as a tumor suppressor in normal conditions and a promoter in cancer highlights its complex involvement in disease.
Area of Science:
- Molecular Biology
- Cell Signaling
- Oncology
Background:
- The transforming growth factor-beta (TGF-β) signaling pathway is crucial for regulating cell behavior.
- It operates via canonical SMAD-mediated and noncanonical pathways (MAPK, PI3K/AKT, Rho-GTPases, NF-κB).
- This pathway is implicated in tissue homeostasis, fibrosis, and cancer progression.
Purpose of the Study:
- To elucidate the dual role of TGF-β signaling in physiological and pathological contexts.
- To detail the involvement of TGF-β in cancer and fibrosis.
- To explore potential theranostic strategies targeting the TGF-β pathway.
Main Methods:
- Review of existing literature on TGF-β signaling mechanisms.
- Analysis of TGF-β's function in normal cell processes.
- Investigation of TGF-β's role in cancer and fibrotic disease development.
Main Results:
- TGF-β signaling acts as a tumor suppressor in normal conditions by promoting quiescence and apoptosis.
- In pathological states like cancer and inflammation, TGF-β promotes tumor progression and fibrosis.
- Interactions between canonical and noncanonical pathways fine-tune TGF-β's complex actions.
Conclusions:
- TGF-β signaling exhibits paradoxical functions, acting as a tumor suppressor or promoter depending on the context.
- The pathway's intricate regulation is key to its diverse roles in health and disease.
- Targeting TGF-β signaling offers potential for novel cancer and fibrosis theranostics.
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