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Exogenous Cx43 expression decrease cell proliferation rate in rat hepatocarcinoma cells independently of functional gap junction

BACKGROUND: Gap junction intercellular communication (GJIC) is considered to play a role in the regulation of homeostasis because it regulates important processes, such as cell proliferation and cell differentiation. A reduced or lost GJIC capacity has been observed in solid tumors and studies have...

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Autores principales: Ionta, Marisa, Ferreira, Raphael Adolpho Sant'ana, Pfister, Sandra Cristina, Machado-Santelli, Gláucia Maria
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2738655/
https://www.ncbi.nlm.nih.gov/pubmed/19678939
http://dx.doi.org/10.1186/1475-2867-9-22
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author Ionta, Marisa
Ferreira, Raphael Adolpho Sant'ana
Pfister, Sandra Cristina
Machado-Santelli, Gláucia Maria
author_facet Ionta, Marisa
Ferreira, Raphael Adolpho Sant'ana
Pfister, Sandra Cristina
Machado-Santelli, Gláucia Maria
author_sort Ionta, Marisa
collection PubMed
description BACKGROUND: Gap junction intercellular communication (GJIC) is considered to play a role in the regulation of homeostasis because it regulates important processes, such as cell proliferation and cell differentiation. A reduced or lost GJIC capacity has been observed in solid tumors and studies have demonstrated that GJIC restoration in tumor cells contribute to reversion of the transformed phenotype. This observation supports the idea that restoration of the functional channel is essential in this process. However, in the last years, reports have proposed that just the increase in the expression of specific connexins can contribute to reversion of the malign phenotype in some tumor cells. In the present work, we studied the effects of exogenous Connexin 43 (Cx43) expression on the proliferative behavior and phenotype of rat hepatocarcinoma cells. RESULTS: The exogenous Cx43 did not increase GJIC capacity of transfected cells, but it was critical to decrease the cell proliferation rate as well as reorganization of the actin filaments and cell flattening. We also observed more adhesion capacity to substrate after Cx43 transfection. CONCLUSION: Cx43 expression leads to a decrease of the growth of the rat hepatocellular carcinoma cells and it contributes to the reversion of the transformed phenotype. These effects were independent of the GJIC and were probably associated with the phosphorylation pattern changes and redistribution of the Cx43 protein.
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spelling pubmed-27386552009-09-05 Exogenous Cx43 expression decrease cell proliferation rate in rat hepatocarcinoma cells independently of functional gap junction Ionta, Marisa Ferreira, Raphael Adolpho Sant'ana Pfister, Sandra Cristina Machado-Santelli, Gláucia Maria Cancer Cell Int Primary Research BACKGROUND: Gap junction intercellular communication (GJIC) is considered to play a role in the regulation of homeostasis because it regulates important processes, such as cell proliferation and cell differentiation. A reduced or lost GJIC capacity has been observed in solid tumors and studies have demonstrated that GJIC restoration in tumor cells contribute to reversion of the transformed phenotype. This observation supports the idea that restoration of the functional channel is essential in this process. However, in the last years, reports have proposed that just the increase in the expression of specific connexins can contribute to reversion of the malign phenotype in some tumor cells. In the present work, we studied the effects of exogenous Connexin 43 (Cx43) expression on the proliferative behavior and phenotype of rat hepatocarcinoma cells. RESULTS: The exogenous Cx43 did not increase GJIC capacity of transfected cells, but it was critical to decrease the cell proliferation rate as well as reorganization of the actin filaments and cell flattening. We also observed more adhesion capacity to substrate after Cx43 transfection. CONCLUSION: Cx43 expression leads to a decrease of the growth of the rat hepatocellular carcinoma cells and it contributes to the reversion of the transformed phenotype. These effects were independent of the GJIC and were probably associated with the phosphorylation pattern changes and redistribution of the Cx43 protein. BioMed Central 2009-08-13 /pmc/articles/PMC2738655/ /pubmed/19678939 http://dx.doi.org/10.1186/1475-2867-9-22 Text en Copyright © 2009 Ionta et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Primary Research
Ionta, Marisa
Ferreira, Raphael Adolpho Sant'ana
Pfister, Sandra Cristina
Machado-Santelli, Gláucia Maria
Exogenous Cx43 expression decrease cell proliferation rate in rat hepatocarcinoma cells independently of functional gap junction
title Exogenous Cx43 expression decrease cell proliferation rate in rat hepatocarcinoma cells independently of functional gap junction
title_full Exogenous Cx43 expression decrease cell proliferation rate in rat hepatocarcinoma cells independently of functional gap junction
title_fullStr Exogenous Cx43 expression decrease cell proliferation rate in rat hepatocarcinoma cells independently of functional gap junction
title_full_unstemmed Exogenous Cx43 expression decrease cell proliferation rate in rat hepatocarcinoma cells independently of functional gap junction
title_short Exogenous Cx43 expression decrease cell proliferation rate in rat hepatocarcinoma cells independently of functional gap junction
title_sort exogenous cx43 expression decrease cell proliferation rate in rat hepatocarcinoma cells independently of functional gap junction
topic Primary Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2738655/
https://www.ncbi.nlm.nih.gov/pubmed/19678939
http://dx.doi.org/10.1186/1475-2867-9-22
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