In continuation of how dietary supplement may block cancer cells... In my earlier blogs, I have mentioned that, sulforaphane and other key ingredient diindolylmethane (natural compound formed during the autolytic breakdown of glucobrassicin present in food plants of the Brassica genus, including broccoli, cabbage, Brussels sprouts, cauliflower and kale) are responsible for the anticancer activity associated with broccoli and other Brassica genus.
Now researchers at the Ohio State University Comprehensive Cancer Center-Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC-James) have discovered how a substance (see below structure) that is produced when eating broccoli and Brussels sprouts can block the proliferation of cancer cells.
Compelling evidence indicates that the substance,
indole-3-carbinol [(above structure, I3C) :
Glucobrassicin (right structure) is a type of
glucosinolate that can be found in almost all cruciferous plants, such as cabbages and broccoli, degradation by the enzyme
myrosinase is expected to produce an isothiocyanate, indol-3-ylmethylisothiocyanate- which is unstable and hydrlyses to give, I3C, as most dominant degradation product], may have anticancer effects and other health benefits, the researchers say. These findings show how I3C affects cancer cells and normal cells.
The laboratory and animal study discovered a connection between I3C and a molecule called
Cdc25A, which is essential for cell division and proliferation. The research showed that I3C causes the destruction of that molecule and thereby blocks the growth of breast cancer cells.
"Cdc25A is present at abnormally high levels in about half of breast cancer cases, and it is associated with a poor prognosis," says study leader Xianghong Zou, assistant professor of pathology at the Ohio State University Medical Center.
For this study, Zou and his colleagues exposed three breast cancer cell lines to I3C. These experiments revealed that the substance caused the destruction of Cdc25A. They also pinpointed a specific location on that molecule that made it susceptible to I3C, showing that if that location is altered (because of a gene mutation), I3C no longer causes the molecule's destruction.
Last, the investigators tested the effectiveness of I3C in breast tumors in a mouse model. When the substance was given orally to the mice, it reduced tumor size by up to 65 percent. They also showed that I3C had no affect on breast-cell tumors in which the Cdc25A molecule had a mutation in that key location.
Ref : American Association for Cancer Research :
Cancer Prevention Research, Xianghong Zou et al.,
