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Updated: Jun 25, 2025

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Published on: October 27, 2020
Cross-Talk between the TGF-β and Cell Adhesion Signaling Pathways in Cancer
Jiahao Liao1,2, Rentang Chen1,2, Bihua Lin1
1Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics, Dongguan Key Laboratory of Medical Bioactive Molecular Developmental and Translational Research, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan, Guangdong, 523808, China.
Abstract:
Transforming growth factor-β (TGF-β) is strongly associated with the cell adhesion signaling pathway in cell differentiation, migration, etc. Mechanistically, TGF-β is secreted in an inactive form and localizes to the extracellular matrix (ECM) via the latent TGF-β binding protein (LTBP). However, it is the release of mature TGF-β that is essential for the activation of the TGF-β signaling pathway. This progress requires specific integrins (one of the main groups of cell adhesion molecules (CAMs)) to recognize and activate the dormant TGF-β. In addition, TGF-β regulates cell adhesion ability through modulating CAMs expression. The aberrant activation of the TGF-β signaling pathway, caused by abnormal expression of key regulatory molecules (such as Smad proteins, certain transcription factors, and non-coding RNAs), promotes tumor invasive and metastasis ability via epithelial-mesenchymal transition (EMT) during the late stages of tumorigenesis. In this paper, we summarize the crosstalk between TGF-β and cell adhesion signaling pathway in cancer and its underlying molecular mechanisms.
Insights
Transforming growth factor-β (TGF-β) signaling interacts with cell adhesion molecules to influence cell behavior. Aberrant TGF-β activation promotes cancer invasion and metastasis through epithelial-mesenchymal transition (EMT).
Area of Science:
- Oncology
- Cell Biology
- Molecular Biology
Background:
- Transforming growth factor-β (TGF-β) is crucial for cell differentiation and migration, interacting with the cell adhesion signaling pathway.
- TGF-β is secreted in an inactive complex and requires release of mature TGF-β for signaling pathway activation.
- Cell adhesion molecules (CAMs), particularly integrins, play a key role in recognizing and activating latent TGF-β.
Purpose of the Study:
- To summarize the crosstalk between TGF-β and cell adhesion signaling in cancer.
- To elucidate the underlying molecular mechanisms of this interaction.
Main Methods:
- Literature review and synthesis of existing research on TGF-β signaling and cell adhesion in cancer.
- Analysis of molecular mechanisms involving integrins, CAMs expression, and regulatory molecules like Smad proteins, transcription factors, and non-coding RNAs.
Main Results:
- TGF-β regulates cell adhesion by modulating CAMs expression.
- Integrins are essential for the release and activation of mature TGF-β.
- Aberrant TGF-β pathway activation, driven by dysregulated molecules, promotes tumor invasion and metastasis via epithelial-mesenchymal transition (EMT).
Conclusions:
- The interplay between TGF-β and cell adhesion signaling is a critical determinant of cancer progression.
- Understanding these molecular mechanisms provides insights into potential therapeutic targets for inhibiting tumor invasion and metastasis.
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