Loss of functional E-cadherin renders cells more resistant to the apoptotic agent taxol in vitro

• Type: Article in International Scientific Journal
• Date: 2005

Authors

Ferreira, P (Author) Other; Oliveira, MJ (Author) Other; Beraldi, E (Author) Other; Mateus, AR (Author) Other; Nakajima, T (Author) Other; Gleave, M (Author) Other; Yokota, J (Author) Other; Carneiro F (Author) FMUP; Huntsman, D (Author) Other; Seruca, R (Author) FMUP; Suriano, G (Author) Other

Journal

Title: Experimental Cell Research

Vol. 310

Pages: 99-104

ISSN: 0014-4827

Publisher: Elsevier

Indexing

ISI Web of Knowledge - 44 Citations

Scopus - 46 Citations

Other information

Authenticus ID: P-000-0XJ

DOI: 10.1016/j.yexcr.2005.07.010

Abstract (EN): 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 antiapoptotic bcl-2 protein.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 6