Sulforaphane’s Role in Preventing Prostate Cancer

Treatment of cancers by chemical agents comes in two types. One is chemotherapy, aimed at affecting the actual cancer and the other is chemo-prevention, aimed at preventing the formation of a cancer. Sulforaphane (SFN) is a chemical being investigated for its role as a chemo-preventive agent. In the current study, sulforaphane was tested in cell lines representing normal prostatic cell, cells from benign hyperplasia and cells of prostatic cancer. It was found that sulforaphane selectively affects the cell cycle in prostatic hyperplasia and prostatic cancers but not the cell cycle in normal prostatic cells. Since sulforaphane is naturally present in cruciferous vegetables such as broccoli, a diet incorporating these vegetables could be a cost-effective way to prevent prostate cancer.

Vegetables such as broccoli and cabbage belong to the family of cruciferous vegetables. It is known that intake of such vegetables may lower the overall risk of prostate cancer. Sulforaphane, a chemical derived from cruciferous vegetables, has multiple actions on cell division. It affects tumor development by cell cycle arrest and by controlling apoptosis. Also, sulforaphane might inhibit a specific enzyme called histone deacetylase (HDAC).This enzyme opens chromatin and facilitates access to DNA — the building block of genetic material. Changes in DNA are implicated in the abnormal cell division and uncontrolled growth that is seen in cancer. By controlling the action of histone deacetylase, the chemicals in cruciferous vegetables may protect cells from becoming cancerous. The current study examined the effects of sulforaphane on normal and cancerous prostate epithelial cell lines in the laboratory.

* Cell lines representing normal prostate epithelial cells, benign prostatic hyperplasia epithelial cells and prostate cancer epithelial cells were cultured and used in the laboratory.
* A few cell lines were treated with a vehicle dimethylsufoxide (DMSO) and acted as a control. Other cell lines were treated with sulforaphane.
* From this material, cell death (apoptosis) effect of sulforaphane on stages of cell cycle, cellular metabolite analysis and quantification of.histone deacetylase (HDAC)  enzyme was performed.
* All experiments were repeated three times. Statistical analysis was then performed.

* After 24 and 48 hours of treatment with sulforaphane, the cell cycle arrest was significant in benign prostate cell lines and prostate cancer cell lines. There was no effect on normal prostate cell lines.
* At 24 hours, the activity of histone deacetylase enzyme was found to be suppressed in all cell lines but this effect was very significant in cancer cell lines than in normal prostate cell lines.
* At 48 hours, the suppression of histone deacetylase enzyme was not noticed in the normal cell lines, but it was evident in cell lines of benign prostate hyperplasia and prostate cancer.
* Sulforaphane can increase both histone H3 acetylation and a-tubulin acetylation. This acetylation prevents access to DNA and thereby impedes copying of DNA proteins. The copying of DNA proteins is an important step in cell division.

Sulforaphane can target cancer cells and act as a chemo-preventive agent. The current study showed that sulforaphane selectively targets benign hyperplasia cells and cancerous prostate cells but does not affect the normal prostate cells. Sulforaphane selectively caused cell cycle arrest and apoptosis, in hyperplastic and cancer prostate cells. The cycle of cell division and death of cells by apoptosis are two major steps that become abnormal in cancerous cells. Cruciferous vegetables naturally contain sulforaphane. Thus, addition of these vegetables could be a safe and relatively non-toxic way of prevention of prostatic cancer. This dietary addition is also simple and affordable.

No shortcomings were reported in the original report.

For More Information:
Differential Effects of Sulforaphane on Cell Cycle in Normal , Hyperplastic and Cancerous Prostate Cells
Molecular Nutrition Food Research. 2011
By John D. Clarke; Anna Hsu; Oregon State University, Corvallis, Oregon

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