Protein kinase C mu 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 mu (PKCmu) expression in prostate cancer. In this study, quantitative ribonuclease protection assay and immunoblot analysis demonstrate down regulation of PKCmu at transcription and translational level, respectively, in AI C4-2 cells compared to its parental androgen dependent (AD) LNCaP prostate cancer cells. Significantly lower PKCmu 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 PKCmu expression is decreased in 100% of AI human prostate cancers. The consistent down regulation of PKCmu in cell line models and human prostate cancer tissues suggests a possible functionally significant role for PKCmu in progression to AI in prostate cancer.

• Authors: Meena Jaggi, Prema S Rao, David J Smith, George P Hemstreet, K C Balaji
• Journal: Biochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 307 Issue 2 Pg. 254-60 (Jul 25 2003) ISSN: 0006-291X [Print] United States
• PMID: 12859948 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Androgens
• Oligonucleotides, Antisense
• protein kinase D
• Protein Kinase C

Topics

• Androgens (metabolism)
• Down-Regulation (physiology)
• Gene Expression Regulation, Neoplastic
• Humans
• Immunohistochemistry
• Male
• Neoplasm Metastasis
• Oligonucleotides, Antisense (metabolism)
• Prostatic Neoplasms (enzymology, pathology)
• Protein Kinase C (genetics, metabolism)
• Tumor Cells, Cultured