Minority International Research Training Research Presentation
January 14, 2005
Global gene expression analysis of primary prostate cancer cells as a means for developing new models for treatment
CSULA MARC U*STAR Scholar
A global gene expression analysis of mRNA from both cancerous
primary prostate cells and benign prostatic hyperplasia (BPH)
cells were carried out to establish new models for the treatment
of prostate cancer, any changes in gene expression observed between
malignant and non-malignant cells should provide new targets for
therapy. The cell lines Schmac 1(BPH), Schmac 4(prostate tumor
cell, Gleason grade: 3), Schmac 5(prostate tumor cell, Gleason
grade: 6), and P4E6(well-differentiated prostate tumor cell) were
used for analysis, all cell-lines had been immortalized with Human
Papillomavirus-E6. Polymerase Chain Reaction (PCR) with GAPD and
ETL-1 primers were used to validate the integrity of the cDNA
using a reverse transcriptase reaction of the total cell RNA.
Affymetrix HU133A human gene arrays were performed to establish
comparative expression levels of genes in the prostate cell lines.
An independent validation of gene expression for telomerase was
performed using PCR due to the arrays' lack of sensitivity towards
the detection of this important cancer-related gene. Preliminary
bioinformatics analysis of the array data using Microsoft Excel
and Madras indicates up-regulation and down-regulation of several
genes involved in pathways of significance in cancer development.
The Regulation of Store Mediated Calcium Entry
The nature of the mechanism-underlying store mediated Ca2+ entry has been investigated in human platelets through a combination of cytoskeletal modifications. Inhibition of actin polymerization by Cytochalasin D or Latrunculin A had a biphasic time-dependent effect on Ca2+ entry, showing an initial potentiation followed by inhibition of Ca2+ entry. Although store regulated Ca2+ entry appears to be widespread, how Ca2+ store depletion leads to Ca2+ entry across the plasma membrane is not understood. Here we present one possible mechanism by which calcium entry is regulated using different pharmacological agonists.