The Journal of Cancer Research reported the effect of capsaicin—a chemical component found in pepper—to prostate cancer cells. Scientists revealed that 80% of prostate cancer cells undergo apoptosis because of capsaicin. The chemical component inhibits the growth of cultured human prostate cancer cells and slows the development of prostate tumors due to human cell lines in mice. Mori et al. (2006) proposed that capsaicin inhibiting NF-kappa Beta activity indicates its effects to some of apoptotic proteins. The authors noted that steroid-activated proteins control the expression of specific growth related genes which are essential in regulating androgen receptors and limiting the growth of prostate cancer cells. The anti-proliferative effect of capsaicin is a dose-dependent manner. That is, increased concentrations of capsaicin freezes more prostate cancer cells in their G0/G1 stage. The authors’ experiment also yields the same result for androgen-independent prostate cancer cells and capsaicin reaction. As expected, capsaicin reduced the amount of androgen receptor produced by tumor cells. However, the molecule did not affect the normal flow of androgen receptor into the nucleus of the cancer cells. This steroid receptor regulates androgen target genes such as prostate specific antigen (PSA). It has been well-elucidated how capsaicin interferes with androgen receptors especially in modified cells which produce excess numbers of androgen receptors. The authors’ showed that capsaicin also limits the production of PSA in the cancer cell lines.
The problem with conveying scientific information to the lay people is that some important scientific concepts tend to be explained in an overly simplistic manner. Because of these circumstances, the wholistic view of a scientific study for instance is not captured. In the news article presented by ScienceDaily—“Pepper Component Hot Enough to Trigger Suicide in Prostate Cancer Cells”—the story was basically focused on results alone. The article failed to present objectives, methods and important discussion points of the study so that people will be able to understand the research and see its relevance to the society. It is also important to be critical about the methods used in the scientific study to determine the credibility of the data produced—the basis of making inferences.
The news article failed to link the essence of capsaicin to immuno-therapy. Mori et al. (2006) noted that capsaicin is the key to the discovery of transient receptor potential cation channel subfamily V (TRVP1). The authors further reported that therapeutic effect of capsaicin in pain disorders are facilitated through the interaction of capsaicin and receptor but the their results for the three TRVP1-inhibitors capsazepine, ruthenium red, and SB366791, yields a negative result for reduction of the inhibitory activity of capsaicin. Consistent to previous reports of Raisinghani, Pabbidi and Premkumar (2005), the results suggested that capsaicin interaction with TRVP1 do not promote anticancer effects. Other mechanisms also linked capsaicin to the production of oxygen radicals (Surh, 2002) and other effects which is mediated by PPARg. However, their results suggested that capsaicin is a potent agent against prostate cancer cells both androgen-sensitive and androgen-independent.
References
American Association for Cancer Research (2006, March 19). Pepper Component Hot Enough To Trigger Suicide In Prostate Cancer Cells. ScienceDaily. Retrieved from: http://www.sciencedaily.com /releases/2006/03/060319150754.htm.
Mori, A., Lehmann, S., O’Kelly, J., Kumagai, T., Desmond, J.C. et al. (2013). Capsaicin, a Component of Red Peppers, Inhibits the Growth of Androgen-Independent, p53 Mutant Prostate Cancer Cells. Cancer Research, 66(6): 3222-3229.
Raisinghani, M., Pabbidi, R.B. and Premkumar, L. S. (2005). Activation of Transient Receptor Potential Vanilloid 1 (TRPV1) by Resiniferatoxin. Journal of Physiology, 567: 771–786.
Surh, Y. J. (2002). More Than Spice: Capsaicin in Hot Chili Peppers Makes Tumor Cells Commit Suicide. Editorial. Journal of the National Cancer Institute, 94(17): 1263-1265.
