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Updated: Jul 11, 2026

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
Published on: October 27, 2020
Transforming growth factor-beta signaling in cancer invasion and metastasis
Suvi-Katri Leivonen1, Veli-Matti Kähäri
1Department of Dermatology, University of Turku, FI-20521 Turku, Finland.
Abstract:
Transforming growth factor-beta (TGF-beta) family members are polypeptides with dual tumor suppressive and oncogenic effects. They signal through serine/threonine kinase receptor complexes, which phosphorylate cytoplasmic mediators, the Smads. Upon phosphorylation, Smads translocate to the nucleus and associate with transcriptional coactivators or corepressors, and regulate the transcriptional activation of various TGF-beta responsive genes. In addition, TGF-beta activates cellular mitogen-activated protein kinase signaling pathways, which crosstalk with Smad signaling and regulate growth, survival and motility of cells. During tumorigenesis, malignantly transformed cells often lose the response to the tumor suppressive effects of TGF-beta, which, in turn, starts to act as an autocrine tumor promoting factor by enhancing cancer invasion and metastasis. In this review, we summarize current view on the role of TGF-beta signaling in tumorigenesis, with emphasis on cancer invasion and metastasis. On the basis of these recent observations, we discuss new therapeutic strategies targeting TGF-beta signaling at distinct levels as a basis for inhibiting tumor growth, angiogenesis, invasion and metastasis.
Insights
Transforming growth factor-beta (TGF-beta) signaling has dual roles in cancer. This review highlights TGF-beta
Area of Science:
- Molecular Biology
- Cancer Research
- Cell Signaling
Background:
- Transforming growth factor-beta (TGF-beta) family members exhibit complex roles in cancer, acting as both tumor suppressors and oncogenes.
- TGF-beta signaling involves serine/threonine kinase receptors, Smad proteins, and crosstalk with mitogen-activated protein kinase pathways.
- Cancer cells often evade TGF-beta's tumor-suppressive functions, leading to its promotion of invasion and metastasis.
Purpose of the Study:
- To review the multifaceted role of TGF-beta signaling in tumorigenesis, focusing on cancer invasion and metastasis.
- To discuss emerging therapeutic strategies targeting TGF-beta signaling pathways for cancer treatment.
Main Methods:
- Literature review of current research on TGF-beta signaling in cancer.
- Analysis of Smad and MAPK pathway interactions in tumorigenesis.
- Examination of TGF-beta's role in cancer cell invasion and metastasis.
Main Results:
- TGF-beta signaling is crucial for regulating cell growth, survival, and motility.
- Loss of TGF-beta responsiveness in cancer promotes invasion and metastasis.
- TGF-beta can act as an autocrine factor to enhance malignant progression.
Conclusions:
- Targeting TGF-beta signaling offers potential therapeutic avenues for inhibiting tumor growth, angiogenesis, invasion, and metastasis.
- Understanding the dual role of TGF-beta is critical for developing effective cancer therapies.
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