Meena Jaggi

Protein kinase C μ is down-regulated in androgen-independent prostate cancer

Abstract Progression to androgen independence (AI) is the main cause of death in prostate cancer. Our prior differential gene expression studies by microarray analysis in progressive prostate cancer cell line model identified dysregulation of protein kinase C μ (PKCμ) expression in prostate cancer. In this study, quantitative ribonuclease protection assay and immunoblot analysis demonstrate down regulation of PKCμ at transcription and translational level, respectively, in AI C4-2 cells compared to its parental androgen dependent (AD) LNCaP prostate cancer cells. Significantly lower PKCμ kinase activity was confirmed in C4-2 cells by in vitro kinase assay. Immunohistochemical studies of prostate cancer tissue from patient progressing to AI prostate cancer demonstrated that PKCμ expression is decreased in 100% of AI human prostate cancers. The consistent down regulation of PKCμ in cell line models and human prostate cancer tissues suggests a possible functionally significant role for PKCμ in progression to AI in prostate cancer.

Differential Displacement of Classical Cadherins by VE-Cadherin

VE-cadherin is an endothelial cell-specific, type II classical cadherin that plays an important role in permeability, vasculogenesis, and vascular remodeling. Endothelial cells express equal levels of VE- and N-cadherin; VE-cadherin is present in junctions while N-cadherin is diffusely expressed over the surface of the cell. The present study was designed first to determine if the ability of VE-cadherin to displace N-cadherin from junctions was endothelial-cell specific, and second to determine if VE-cadherin could displace other classical cadherins from cell junctions. Our data suggest that VE-cadherin specifically influences the cellular localization of N-cadherin, independent of cell type, and does not effect the localization of other classical cadherins.

PKD1 (protein kinase D1)

Review on PKD1 (protein kinase D1), with data on DNA, on the protein encoded, and where the gene is implicated.