victor hugo lopez diaz - Academia.edu (original) (raw)
Docente Maestría en Gerencia y auditoria tributaria Coordinador de investigación. Investigador Senior
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UERJ - Universidade do Estado do Rio de Janeiro / Rio de Janeiro State University
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Papers by victor hugo lopez diaz
Zenodo (CERN European Organization for Nuclear Research), Mar 30, 2023
Journal of Biological …, 1998
The phorbol ester phorbol 12-myristate 13-acetate induces remarkable phenotypic changes in intest... more The phorbol ester phorbol 12-myristate 13-acetate induces remarkable phenotypic changes in intestinal HT-29 M6 cells; these changes consist of loss of homotypic adhesion and inactivation of E-cadherin. In parallel, cell growth is retarded. We have transfected HT-29 M6 cells with an activated form of the conventional protein kinase C␣ (cPK-C␣). Expression of this isoform induced the acquisition of a scattered phenotype, similar to that adopted by cells after addition of phorbol 12myristate 13-acetate, with very low cell-to-cell aggregation and undetectable levels of functional E-cadherin. These cell clones were highly motile and rapidly invaded embryonic chick heart fragments. Furthermore, cells expressing activated-cPK-C␣ showed decreased proliferation in comparison to control clones. We have also studied how these two apparently antagonistic changes affect the tumorigenic ability of HT-29 M6 cells. When the different cell clones were xenografted into athymic mice, the effect on cell growth seemed to predominate. Expression of activated-cPK-C␣ significantly reduced the size of the tumors; the cells with the highest level of expression did not even form subcutaneous tumors. Besides their smaller size, the morphology of these tumors was clearly different from those originated by HT-29 M6 cells, and they could be defined as infiltrative on anatomo-pathological basis. These results indicate that cPK-C␣ controls both cell-to-cell adhesion and proliferation of intestinal cells. * This research was supported by Grants SAF94-1008 and SAF97-0080 from the Fundación Ramón Areces and Comisión Interministerial de Ciencia y Tecnología (to A. G. d. H.) and by Grant GRQ 93-9301 from Comissió Interdepartamental de Recerca i Tecnologia to the Unitat de Biologia Cellular i Molecular. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. ‡ Predoctoral fellowship from CIRIT (Generalitat de Catalunya). § Supported by funds from La Marató de TV3. ¶ Predoctoral fellowship from Ministerio de Educación. ʈ Supported by Fundación Ramón Areces.
Zenodo (CERN European Organization for Nuclear Research), Mar 30, 2023
Journal of Biological …, 1998
The phorbol ester phorbol 12-myristate 13-acetate induces remarkable phenotypic changes in intest... more The phorbol ester phorbol 12-myristate 13-acetate induces remarkable phenotypic changes in intestinal HT-29 M6 cells; these changes consist of loss of homotypic adhesion and inactivation of E-cadherin. In parallel, cell growth is retarded. We have transfected HT-29 M6 cells with an activated form of the conventional protein kinase C␣ (cPK-C␣). Expression of this isoform induced the acquisition of a scattered phenotype, similar to that adopted by cells after addition of phorbol 12myristate 13-acetate, with very low cell-to-cell aggregation and undetectable levels of functional E-cadherin. These cell clones were highly motile and rapidly invaded embryonic chick heart fragments. Furthermore, cells expressing activated-cPK-C␣ showed decreased proliferation in comparison to control clones. We have also studied how these two apparently antagonistic changes affect the tumorigenic ability of HT-29 M6 cells. When the different cell clones were xenografted into athymic mice, the effect on cell growth seemed to predominate. Expression of activated-cPK-C␣ significantly reduced the size of the tumors; the cells with the highest level of expression did not even form subcutaneous tumors. Besides their smaller size, the morphology of these tumors was clearly different from those originated by HT-29 M6 cells, and they could be defined as infiltrative on anatomo-pathological basis. These results indicate that cPK-C␣ controls both cell-to-cell adhesion and proliferation of intestinal cells. * This research was supported by Grants SAF94-1008 and SAF97-0080 from the Fundación Ramón Areces and Comisión Interministerial de Ciencia y Tecnología (to A. G. d. H.) and by Grant GRQ 93-9301 from Comissió Interdepartamental de Recerca i Tecnologia to the Unitat de Biologia Cellular i Molecular. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. ‡ Predoctoral fellowship from CIRIT (Generalitat de Catalunya). § Supported by funds from La Marató de TV3. ¶ Predoctoral fellowship from Ministerio de Educación. ʈ Supported by Fundación Ramón Areces.