Several studies over the last few years have found a possible connection between the consumption of the spice turmeric and it's active component, curcumin, and reduced risk of certain cancers. A recent study published in the journal Cancer Research by University of Alabama researchers helps to "identify a mechanism by which curcumin functions as an anticancer agent."1
In the study, the researchers cultivated a strain of human prostate cancers cells, known as PC-3, in vitro. To directly test the effect of curcumin on these cancers, curcumin was added to the medium. The researchers found that the curcumin worked in two different ways to inhibit cancer growth. The curcumin inhibited a protein called MDM2 that plays a critical rule in stimulating tumor growth. At the same time the curcumin stimulated a different protein called p21 that suppresses cancer through apoptosis (cell death) of the cancer cells.
Moving forward with what they had already learned, the researchers grafted PC-3 cancer cells in to a group of hairless mice. Once the cancer was established in the mice, they were given either curcumin or cottonseed oil as a placebo 5 days a week for 4 weeks. The test mice that had received the curcumin were then divided again into 3 groups and given different treatments. One group only received the curcumin, the second group received curcumin plus a chemotherapy drug gemcitabine, and the third group received curcumin and radiation treatments.
The researchers found that all three curcumin treatments inhibited the growth of the PC-3 cell grafts and that the curcumin enhanced the effects chemotherapy and radiotherapy. The researchers went on to suggest that future researcher was need to investigate the potential of adding curcumin to traditional cancer treatment in various human cancers that use the MDM2 pathway, such as prostate and colorectal.
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1. Li, M., Z. Zhang, et al. (2007). "Curcumin, a dietary component, has anticancer, chemosensitization, and radiosensitization effects by down-regulating the MDM2 oncogene through the PI3K/mTOR/ETS2 pathway." Cancer Res 67(5): 1988-96.