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

Jean-Carlo Roncagliolo

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

Jaime Angiano
CSULA Undergraduate

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.