Departmental Affiliation and City, State, Zip for All Authors

Department of Biology, Xavier University of Louisiana, New Orleans, Louisiana 70125; Institute for Molecular Medicine, University of North Texas Health Science Center, Fort Worth, Texas 76107

Scientific Abstract

Cancer can develop due to an increase in cell proliferation or a decrease in cell death. Cellular pathways are deregulated in cancer, which allows for the proliferation of cells. The Protein Kinase C (PKC) family of proteins regulates cell proliferation, differentiation, and cell death. There are three subgroups of PKCs: conventional, novel, and atypical. PKCeta is a member of the novel PKC family, but its regulation is distinct from other novel members of the PKC family. It is the only PKC isoform that is upregulated by tumor-promoting phorbol esters. The purpose of the present study was to determine how PKCeta regulates cell proliferation in breast cancer cells. MCF-7 breast cancer cells were used in the study. The levels of PKCeta and other proteins were determined by western blot analysis. Cell survival was monitored by clonogenic assay. PKCeta knockdown decreased clonogenic cell survival of MCF-7 breast cancer cells. The overexpression of PKCeta caused an increase in clonogenic cell survival of MCF-7 breast cancer cells. The level of phosphorylated extracellular signal-regulated kinase (P-ERK), but not total ERK, was increased by PKCeta overexpression. Thus, our study suggests that PKCeta regulates cell proliferation through ERK.

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REGULATION OF CELL PROLIFERATION BY PROTEIN KINASE C-ETA IN BREAST CANCER CELLS

Cancer can develop due to an increase in cell proliferation or a decrease in cell death. Cellular pathways are deregulated in cancer, which allows for the proliferation of cells. The Protein Kinase C (PKC) family of proteins regulates cell proliferation, differentiation, and cell death. There are three subgroups of PKCs: conventional, novel, and atypical. PKCeta is a member of the novel PKC family, but its regulation is distinct from other novel members of the PKC family. It is the only PKC isoform that is upregulated by tumor-promoting phorbol esters. The purpose of the present study was to determine how PKCeta regulates cell proliferation in breast cancer cells. MCF-7 breast cancer cells were used in the study. The levels of PKCeta and other proteins were determined by western blot analysis. Cell survival was monitored by clonogenic assay. PKCeta knockdown decreased clonogenic cell survival of MCF-7 breast cancer cells. The overexpression of PKCeta caused an increase in clonogenic cell survival of MCF-7 breast cancer cells. The level of phosphorylated extracellular signal-regulated kinase (P-ERK), but not total ERK, was increased by PKCeta overexpression. Thus, our study suggests that PKCeta regulates cell proliferation through ERK.

Manuscript Number

1009