PKC inhibition increases gap junction intercellular communication and cell adhesion in human neuroblastoma.
Cell Tissue Res
; 340(2): 229-42, 2010 May.
Article
em En
| MEDLINE
| ID: mdl-20336469
ABSTRACT
Gap junction intercellular communication and cell-cell adhesion are essential for maintaining a normal cellular phenotype, including the control of growth and proliferation. Loss of either cell-cell adhesion or communication is common in cancers, while restoration of function is associated with tumor suppression. Protein kinase C (PKC) isozymes regulate a broad spectrum of cellular functions including growth and proliferation, and their overexpression has been correlated with carcinogenesis. Consequently, PKC inhibitors are currently undergoing clinical trials as an anti-cancer agents although the precise cellular alterations induced by PKC inhibitors remain to be elucidated. In the current study, the effects of PKC inhibitors on cell interactions were investigated using human neuroblastoma (IMR32, SKNMC, and SHSY-5Y) cell lines. An analysis of intercellular communication revealed an increase in gap junctional coupling with PKC inhibition. The observed increase in coupling was not associated with a change in Connexin 43 distribution or an alteration of phosphorylation status of the protein. There was also an increase in cell-cell adhesion with PKC inhibitor treatment as indicated by a cell aggregation assay. Therefore, the growth suppressive abilities of PKC inhibition on tumors may be due to the cancer suppressive effects of increased gap junction intercellular communication and cell-cell adhesion.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Proteína Quinase C
/
Comunicação Celular
/
Junções Comunicantes
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Neuroblastoma
Limite:
Humans
Idioma:
En
Revista:
Cell Tissue Res
Ano de publicação:
2010
Tipo de documento:
Article
País de afiliação:
Canadá