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PKC, KEY SWITCH IN CANCER SIGNALING PATHWAYS
Autores:
MARIA TERESA CORONADO PARRA
,
CONSOLACION MARIN VICENTE
,
SONIA REVERTE RÓDENAS
, EMILIO SERRANO LOPEZ,
JUAN CARMELO GÓMEZ FERNÁNDEZ
,
MARIA SENENA CORBALÁN GARCÍA
,
Grupos de investigación:
[GI/IMIB/C070/2011] Biomembranas y Señalización Celular
Comunicación:
Antecedentes:
Cancer cells show a great versatility in signal transduction pathways. One of the groups of proteins involved in these cellular processes is the family of Protein Kinase C. These enzymes phosphorylate their targets in residues of serine or threonine and have been implicated in a myriad of processes important to tumour progression such as proliferation, migration or apoptosis. They are ubiquitous and regulated by phosphorylation, interaction with other proteins and different cofactors such as Ca2+ and lipids. Depending on the isoenzyme and the cellular type, their involvement can be pro-oncogenic or anti-oncogenic. So far, no efficient therapy based on the use of these proteins has been developed for impairing tumorigenesis.
Métodos:
In the present work, we use transcriptomics to study the effect of supressing the expression of classical PKC alpha in breast cancer model cells. The Estrogen Receptor+ and Progesterone Receptor+ MCF7 cells were knocked down in PKC alpha by using siRNA technology.
Resultados:
A total of 13461 unique mRNA transcripts were analyzed in an Affymetrix microarray. Among them, 168 probes were significantly up-regulated and 79 probes were down-regulated. Gene Ontology analyses in several databases identified down-regulated genes of the MAPK and ErbB families, while the up-regulated genes rendered inositol phosphate metabolism and phosphatidylinositol signalling as the most important groups.
Conclusiones:
These results indicate that PKC? is directly involved in the oncogenic process by controlling key regulatory pathways. Furthermore, its down-regulation promotes the over-expression of many other proteins indicating that PKC? might act as a break to control their activity.
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