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Involvement of integrins in cell survival
R C Bates1, L F Lincz, G F Burns
1Cancer Research Unit, Faculty of Medicine, University of Newcastle, NSW, Australia.
Cancer Metastasis Reviews
|September 1, 1995
Summary
The extracellular matrix regulates apoptosis through integrin signaling. Loss of cell adhesion to the ECM can trigger cell death, impacting cancer development.
Area of Science:
- Cell Biology
- Biochemistry
- Oncology
Background:
- Apoptosis is a crucial regulated cell death process for maintaining homeostasis in multicellular organisms.
- Dysregulation of apoptosis contributes to oncogenesis.
- The extracellular matrix (ECM) is increasingly recognized for its role in regulating apoptosis, with integrins as key signal transmitters.
Purpose of the Study:
- To explore the role of the extracellular matrix (ECM) and integrin signaling in regulating apoptosis.
- To understand how ECM-ECM and cell-cell interactions influence apoptosis.
- To identify downstream mechanisms of integrin-mediated apoptosis.
Main Methods:
- Investigating the effects of ECM component adhesion and integrin binding on apoptosis.
- Analyzing the role of cell-cell adhesion in preventing apoptosis.
- Examining downstream signaling pathways, including ICE transcription and p53 nuclear translocation.
Main Results:
- Loss of adhesion to ECM components can induce apoptosis, which can be experimentally triggered by blocking integrin binding.
- Both heterotypic and homotypic cell-cell adhesion can protect against adhesion-dependent apoptosis, often mediated by integrins.
- Integrin signaling can promote apoptosis, with potential downstream mechanisms involving ICE and p53.
Conclusions:
- Alterations in integrin expression or signaling can promote tumor development by allowing cells to evade apoptosis.
- Cell-cell adhesion plays a significant role in tumor cell survival.
- Targeting ECM-integrin interactions and cell-cell adhesion presents potential therapeutic strategies for malignancy.