While the normal healthy cells within our body are destined to die after a predetermined number of cell divisions (senescence), cancer cells are, essentially, immortal. They divide endlessly, until enough cancer cells have formed to cause a tumor. Similarly the normal cells that line your colon (as well as all of the other estimated 75 trillion cells that make up the human body) never decide to leave the colon and spread to, say, your liver or your lungs. However, colon cancer cells seem to have an overwhelming compulsion to move into blood vessels and lymphatic vessels, and from there, to spread to other distant organs of the body. Once these nefarious pioneers arrive in the liver, the lungs, or in other organs outside of the colon, these metastatic tumor cells then resume their growth cycle, eventually causing metastatic tumors to form. Other types of cancer exhibit the same malignant biology, beginning with invasion through normal tissues, followed by invasion into blood vessels or lymphatic vessels, and ending with the establishment of metastatic colonies of tumors in distant organs and tissues.
This unique, and potentially deadly, biology of cancer cells arises from hundreds, if not thousands, of genetic mutations and other transforming events that occur within cancer cells. As we are still in the infancy of our understanding of the complex biology of cancer cells, we are only beginning to understand the interplay between these hundreds, if not thousands, of aberrations in cancer cell biology.
In most cancer cells, genes that play important roles in normal cell growth and division become corrupted, either due to genetic mutations that cause these “tumor suppressor genes” to become inactivated, or through other so-called “epigenetic” alterations that can also inactivate tumor suppressor genes. One such epigenetic mechanism whereby tumor suppressor genes are commonly inactivated is through “hypermethylation” of the promoter region of the gene.
The promoter region of genes can be thought of as a switch that turns on the activation of a gene to produce its specific protein product. Hypermethylation is a process whereby the promoter region of a gene is essentially locked into the “off position.” (When gene hypermethylation occurs, the affected gene is said to be “silenced.”)
Tumor suppressor genes produce proteins that reduce the risk of normal cells becoming cancer cells. Therefore, when key tumor suppressor genes are silenced by hypermethylation, normal (benign) cells may become transformed into malignant cells. This very basic review of the molecular biology of tumor suppressor genes and carcinogenesis is important in order to understand this week’s featured research study.
A tumor suppressor gene known as BTG3 is known to be commonly silenced, by hypermethylation of its promoter region, in cancers of the prostate, breast and kidney. There also is experimental evidence showing that genistein, which is a dietary nutrient found in soybeans and soybean products, can reverse the hypermethylation of multiple different tumor suppressor genes, including BTG3. (Once hypermethylation is reversed, the gene is once again able to produce its cancer-preventing protein.)
A new research study, just published in the journal Cancer, evaluated the effects of genistein on hypermethylated human prostate cancer cells. In this elegant laboratory study, prostate cancer cells were grown in culture dishes, and were tested for hypermethylation of the BTG3 tumor suppressor gene. Once the scientists confirmed that the BTG3 gene was indeed silenced by hypermethylation in these prostate cancer cells, the cells were then treated with genistein. Following additional experiments, the scientists were able to confirm that genistein effectively reversed hypermethylation of the BTG3 tumor suppressor gene. Additionally, a new experimental prostate cancer drug which is being evaluated in ongoing clinical research trials, 5Aza-C, was also tested on the hypermethylated prostate cancer cells, and was found to reverse hypermethylation of the BTG3 tumor suppressor gene, as well.
While it is still a big stretch to assume that the reactivation of the BTG3 tumor suppressor gene in prostate cancer cells growing in a culture dish will translate into clinically meaningful results in human beings, the results of this interesting little study are both intriguing and encouraging. Given that genistein is a natural and generally non-toxic dietary nutrient, it may have certain advantages over the novel prostate cancer drug 5Aza-C (assuming, of course, that ongoing clinical research trials identify a clinical benefit in prostate cancer patients undergoing treatment with 5Aza-C).
The true role of genistein in the prevention and treatment of certain cancers, if any, is not clear at this time. However, the results of this laboratory study add to the growing body of research suggesting that genistein may have clinically significant anti-cancer effects in at least some human cancers.
Dr. Wascher is an oncologic surgeon, a professor of surgery, a cancer researcher, an oncology consultant, and a widely published author
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