Curcumin, the yellow pigment found in the spice turmeric and a key ingredient in yellow curry inhibits melanoma cell growth and stimulates tumor cell death, according to a new study. Published in the August 15, 2005 issue of CANCER (http://www.interscience.wiley.com/cancer-newsroom), a peer-reviewed journal of the American Cancer Society, the study also elucidates curcumin's intracellular mechanisms of action in this type of tumor.
As well as showing antioxidant and anti-inflammatory effects, curcumin has been shown to have anti-cancer properties. In other tumors, it has been demonstrated to inhibit tumor growth and stimulate apoptosis, an intracellular mechanism for cells of all types to "kill" themselves. To evaluate the compound's efficacy in melanoma, researchers led by Razelle Kurzrock, M.D. of the University of Texas M. D. Anderson Cancer Center in Houston treated three melanoma cell lines with curcumin at different doses and for different duration.
Results show that curcumin treatment decreased cell viability in all three cell lines in a dose-dependent manner. Moreover, curcumin induced apoptosis in tumor cells at high concentrations for short periods of time and low concentrations for long periods of time--a new finding in the study of curcumin.
Curcumin was found to suppress two specific proteins normally part of an intracellular pathway that prevents apoptosis when stimulated. Curcumin partially inhibited NF-ęB and strongly inhibited its upstream stimulator and another independent inhibitor of apoptosis, IKK. However, it did not suppress two other signaling pathways associated with melanomas and tumor proliferation, B-Raf/MEK/ERK and Akt pathways.
"Based on our studies, we conclude the curcumin is a potent suppressor of cell viability and inducer of apoptosis in melanoma cell lines," said the authors, adding "Future investigation to determine the effects of curcumin in animal models of melanoma and clinical trials are planned."
Source: Eurekalert & othersLast reviewed: By John M. Grohol, Psy.D. on 21 Feb 2009
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