Apoptosis Cadherins Regulate Cell Survival

Cell-matrix and cell-cell adhesions are important regulators of cell survival. Modulation of either can result in tumor formation and metastasis. The former is regulated by cell-surface integrins, whereas contact between adjacent cells is mediated by cell-surface cadherins. How cadherins control cell survival has not been clear. Increased expression of N-cadherin has been associated with increased invasiveness and cell survival of some carcinomas. Tran et al. report that this may be due stabilization of the antiapoptotic protein Bcl-2. In the absence of integrin-mediated adhesion and growth factors, prostate carcinoma cells in suspension suppressed cell death. This was dependent on cell-cell adhesion through N-cadherin and correlated with increased activation of phosphatidylinositol 3-kinase and the serine-threonine kinase Akt. Intercellular adhesion also induced increased Bcl-2 expression. The survival pathway initiated by integrins also converges on Akt, which suggests overlap between the two adhesion-dependent pathways.

N. L. Tran, D. G. Adams, R. R. Vaillancourt, R. L. Heimark, Signal transduction from N-cadherin increases Bcl-2. J. Biol. Chem. 277, 32905-32914 (2002). [Abstract] [Full Text]

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Signal Transduction from N-cadherin Increases Bcl-2. REGULATION OF THE PHOSPHATIDYLINOSITOL 3-KINASE/Akt PATHWAY BY HOMOPHILIC ADHESION AND ACTIN CYTOSKELETAL ORGANIZATION

Nhan L. Tran, Deanna G. Adams, Richard R. Vaillancourt, and Ronald L. Heimark (30 August 2002)
J. Biol. Chem. 277 (36), 32905. [DOI: 10.1074/jbc.M200300200]
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