The study investigates the impact of cell-matrix interactions on apoptosis, a process crucial for maintaining appropriate cell number and tissue organization. The authors introduce the concept of "anoikis," a form of apoptosis induced by the disruption of interactions between normal epithelial cells and the extracellular matrix. Key findings include: 1. **Anoikis Induction**: Disruption of cell-matrix interactions in two model epithelial cell lines (MDCK and HaCat) induced apoptosis, characterized by DNA fragmentation and nuclear changes. 2. **Regulation of Anoikis**: The acquisition of anchorage-independent or motile phenotypes, such as transformation or treatment with cell motility factors, conferred resistance to anoikis. Conversely, reverse-transformation, which involves the loss of anchorage-independent growth potential, increased sensitivity to anoikis. 3. **Cell-Cell Interactions**: Interactions between cells also modulated their sensitivity to anoikis. Low cell density, treatment with the phorbol ester TPA, and scatter factor all increased resistance to anoikis. 4. **Fibroblasts**: Fibroblasts, which lack intercellular adhesions, were resistant to anoikis, suggesting that anoikis is a cell type-specific property. The study suggests that anoikis is a new function of cell-matrix interactions, potentially playing a role in maintaining tissue structure and controlling cell numbers. The results also highlight the importance of cell-cell interactions and the involvement of proteins like bcl-2 in regulating anoikis.The study investigates the impact of cell-matrix interactions on apoptosis, a process crucial for maintaining appropriate cell number and tissue organization. The authors introduce the concept of "anoikis," a form of apoptosis induced by the disruption of interactions between normal epithelial cells and the extracellular matrix. Key findings include: 1. **Anoikis Induction**: Disruption of cell-matrix interactions in two model epithelial cell lines (MDCK and HaCat) induced apoptosis, characterized by DNA fragmentation and nuclear changes. 2. **Regulation of Anoikis**: The acquisition of anchorage-independent or motile phenotypes, such as transformation or treatment with cell motility factors, conferred resistance to anoikis. Conversely, reverse-transformation, which involves the loss of anchorage-independent growth potential, increased sensitivity to anoikis. 3. **Cell-Cell Interactions**: Interactions between cells also modulated their sensitivity to anoikis. Low cell density, treatment with the phorbol ester TPA, and scatter factor all increased resistance to anoikis. 4. **Fibroblasts**: Fibroblasts, which lack intercellular adhesions, were resistant to anoikis, suggesting that anoikis is a cell type-specific property. The study suggests that anoikis is a new function of cell-matrix interactions, potentially playing a role in maintaining tissue structure and controlling cell numbers. The results also highlight the importance of cell-cell interactions and the involvement of proteins like bcl-2 in regulating anoikis.