Loss of functional E-cadherin renders cells more resistant to the apoptotic agent taxol in vitro
- Instituto de Patologia e Imunologia Molecular da Universidade do Porto (IPATIMUP), 4200 Porto (Portugal)
- Prostate Centre, Vancouver General Hospital, Vancouver, BC (Canada)
- Department of Tumor Pathology, Gunma University Graduate School of Medicine, Gunma (Japan)
- Biology Division, National Cancer Center Research Institute, Tokyo (Japan)
- Genetic Pathology Evaluation Centre of the Department of Pathology and Prostate Centre at Vancouver General Hospital, Department of Pathology, British Columbia Cancer Agency and University of British Columbia, Vancouver (Canada)
- Instituto de Patologia e Imunologia Molecular da Universidade do Porto (IPATIMUP), 4200 Porto (Portugal) and Genetic Pathology Evaluation Centre of the Department of Pathology and Prostate Centre at Vancouver General Hospital, Department of Pathology, British Columbia Cancer Agency and University of British Columbia, Vancouver (Canada)
Experimental evidence supports a role for E-cadherin in suppressing invasion, metastasis, and proliferation. Germline mutations of the E-cadherin represent the genetic cause of hereditary diffuse gastric cancer (HDGC). In this type of tumor, isolated cancer cells permeate the basal membrane and paradoxically survive in the gastric wall in the absence of contact with neighbor epithelial cells or with the extracellular matrix. This suggests that upon E-cadherin deregulation, cells acquired resistance to apoptosis. To test this hypothesis, CHO cells stably expressing either wild-type E-cadherin or the HDGC-related germline mutations T340A and V832M were seeded either on a thin layer of collagen type I or on plastic and then subjected to the apoptotic agent taxol. We found that in vitro functional E-cadherin renders cells more sensitive to the effect of taxol. Our results also indicate that this effect is associated to decreased level of the anti-apoptotic bcl-2 protein.
- OSTI ID:
- 20717667
- Journal Information:
- Experimental Cell Research, Vol. 310, Issue 1; Other Information: DOI: 10.1016/j.yexcr.2005.07.010; PII: S0014-4827(05)00329-0; Copyright (c) 2005 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0014-4827
- Country of Publication:
- United States
- Language:
- English
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