Vitamin D3 modulated gene expression patterns in human primary normal and cancer prostate cells
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Laser-capture Microdissection of Human Prostatic Epithelium for RNA Analysis
Published on: November 26, 2015
Meral Guzey1, Jianhua Luo, Robert H Getzenberg
1Department of Urology, University of Pittsburgh, Pittsburgh, Pennsylvania 15232, USA.
Abstract:
The vitamin D receptor (VDR) is a member of the steroid/retinoid receptor superfamily of nuclear receptors and has potential tumor-suppressive functions in prostate and other cancer types. Vitamin D3 (VD3) exerts its biological actions by binding within cells to VDR. The VDR then interacts with specific regions of the DNA in cells, and triggers changes in the activity of genes involved in cell division, cell survival, and cellular function. Using human primary cultures and the prostate cancer (PCa) cell line, ALVA-31, we examined the effects of VD3 under different culture conditions. Complete G0/G1 arrest of ALVA-31 cells and approximately 50% inhibition of tumor stromal cell growth was observed. To determine changes in gene expression patterns related to VD3 activity, microarray analysis was performed. More than approximately 20,000 genes were evaluated for twofold relative increases and decreases in expression levels. A number of the gene targets that were up- and down-regulated are related to potential mechanisms of prostatic growth regulation. These include estrogen receptor (ER), heat shock proteins: 70 and 90, Apaf1, Her-2/neu, and paxillin. Utilizing antibodies generated against these targets, we were able to confirm the changes at the protein level. These newly reported gene expression patterns provide novel information not only potential markers, but also on the genes involved in VD3 induced apoptosis in PCa.
Insights
Vitamin D3 (VD3) shows tumor-suppressive effects in prostate cancer (PCa) by arresting cancer cell division and inhibiting stromal cell growth. VD3 influences gene expression, impacting cell growth and survival pathways.
Area of Science:
- Oncology
- Molecular Biology
- Endocrinology
Background:
- The vitamin D receptor (VDR) is a nuclear receptor with potential tumor-suppressive roles.
- Vitamin D3 (VD3) mediates its effects through VDR binding, influencing gene activity.
- Prostate cancer (PCa) is a significant health concern where VDR's role is being investigated.
Purpose of the Study:
- To investigate the effects of VD3 on prostate cancer cells (ALVA-31) and tumor stromal cells.
- To identify gene expression changes induced by VD3 in PCa.
- To confirm VDR-mediated gene expression alterations at the protein level.
Main Methods:
- Utilized human primary cultures and the ALVA-31 PCa cell line.
- Performed microarray analysis to assess global gene expression changes (>20,000 genes).
- Validated gene expression changes at the protein level using specific antibodies.
Main Results:
- Observed complete G0/G1 arrest in ALVA-31 cells and ~50% inhibition of tumor stromal cell growth.
- Identified significant up- and down-regulation of genes involved in prostatic growth regulation, including estrogen receptor (ER), heat shock proteins (HSPs) 70 and 90, Apaf1, Her-2/neu, and paxillin.
- Confirmed changes in target protein expression.
Conclusions:
- VD3 exhibits anti-proliferative effects on PCa and associated stromal cells.
- VD3 modulates key genes involved in prostate cancer growth and survival.
- Identified novel gene expression patterns and potential protein markers associated with VD3-induced apoptosis in PCa.
