Dissociation between androgen responsiveness for malignant growth vs. expression of prostate specific differentiation markers PSA, hK2, and PSMA in human prostate cancer models

Citations Over TimeTop 10% of 2003 papers

Abstract

Androgen can coordinately regulate both the tumor growth and expression of prostate specific marker genes as observed for the LAPC-4 human prostate cancer cells. Such coordinated regulation, however, is not universal. In all of the other cell lines, there is a dissociation between androgen responsive regulation of malignant growth vs. regulation of expression of prostate specific markers PSA and hK2. In addition, PSMA activity in these cell lines increases as cells become more androgen independent for growth in vivo. These results emphasize that tumor growth and the expression of the specific secretory genes are independently regulated molecular events even if they share a requirement for androgen and/or AR function. Additional independent mechanisms occur in prostate cancer cells for regulation of expression for even the highly related PSA and hK2 genes. Further studies are needed to clarify the mechanisms for androgen ligand-independent, AR-dependent regulation of the genes that directly effect the growth of androgen (i.e., ligand) independent prostate cancer cells. Unfortunately, the data in this present report do not validate the use of the PSA or hK2 gene as surrogates for a model system for such critically important mechanistic studies. Prostate prostate cancer cells. Unfortunately, the data in this present report do not validate the use of the PSA or hK2 gene as surrogates for a model system for such critically important mechanistic studies.

Related Papers

• → Switch from antagonist to agonist of the androgen receptor blocker bicalutamide is associated with prostate tumour progression in a new model system(1999)420 cited
• → p-Carborane-based androgen antagonists active in LNCaP cells with a mutated androgen receptor(2011)27 cited
• → Methylation dependent miR-510 in prostate cancer: A novel upcoming candidate for prostate cancer(2016)4 cited
• → Development of a New Approach for the Therapy of Prostate Cancer with SPOP Mutations(2015)3 cited
• Cell growth promoting of the androgen receptor mutation(2006)