How Wasabi Kills Cancer.
Scientific researchers already knew that a chemical found in Wasabia japonica and to lesser extent in other related vegetables, called Isothiocyanate, appeared to stop the growth of cancer by causing apoptosis, or cell death, in cancer cells. But researchers didn’t know why, and because they didn’t know how, science was unable to confirm that Wasabia japonica killed cancer cells.
Now though, recent research at Georgetown University found that these vegetable Isothiocyanates sticks to a defective protein found in cancerous cells through the tubulin. The Isothiocyanate chemical only binds to the protein when it is defective, and the protein is only defective when the cell is cancerous. The normal protein and cell are left alone.
Production of the protein in question is controlled by the gene p53. It normally helps stop a cell from replicating uncontrollably, but when the gene p53 is mutated, the protein comes out defective. Not only that, cells with mutated p53 genes are more resistant to chemical cancer treatments, but not to the Wasabia japonica Isothiocyanates.
P53 mutations occur in half of all human cancers, including lung, breast and colon.
Eating Wasabia japonica may help reduce cancer risks because the presence of the vegetable Isothiocyanates was observed to increase the death rate of cancer cells with the p53 mutation.
Researchers found that after the Wasabia japonica chemical, Isothiocyanate, bound to the defective p53 protein, breast cancer cells died. One reason for this may be that the mutated gene also makes the cancerous cells vulnerable to toxic effects from Isothiocyanate that normal cells are resistant to.
Isothiocyanates (ITCs) derived from cruciferous vegetables induce apoptosis in cancer cells. The researchers demonstrated that certain naturally occurring ITCs found in Wasabia japonica selectively deplete mutant p53 and do so via a transcription-independent mechanism. Direct p53 binding followed by conformational changes appears to be a mechanism by which mutant p53 is depleted. Structure−activity relationship studies (SARs) using naturally occurring and synthetic ITCs show that depletion is influenced by the size and shape of the ITC.
Collectively, this study shows that mutant p53 depletion may be an important novel target for cancer chemoprevention and therapy by natural ITCs.
In this study, it was found that ITCs can strongly reduce mutant p53 protein in a variety of cancer cells in a time and dose dependent manner. Reduction of mutant p53 may be important in cancer prevention because ITCs appear to suppress gain-of-function properties through mutant p53 depletion. Also, reduction of mutant p53 may lower drug resistance and lead to new strategies for treating cancer in the clinic, or even at home.
Other studies have shown that inhibition of mutant p53 sensitizes cancer cells to chemotherapeutic agent induced cell death in vitro and in vivo. It was found in human lung, breast, and colon cancer cells that mutant p53 confers cells with increased sensitivity to ITC induced cytotoxicity.
Pretreatment of cells with tubulin binding agents, for example, Taxol, diminishes the binding by ITCs and consequently the downstream effects. This implies that the consumption of Wasabia japonica as a preventative measure is a better option than consuming Wasabia japonica when taking Taxol or similar medication.
The studies support that binding to mutant p53 may constitute an important step for its depletion by ITCs.
Once again, science has shown (at least in part) we are what we eat, and we obviously need to eat more Wasabia japonica.
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