DESCRIPTION (Applicant's Description) The relatively long latency period of
the promotion stage of carcinogenesis represents a window of opportunity
during which dietary factors with chemopreventive potential can inhibit the
process of carcinogenesis. There is substantial evidence supporting a role
for consumption of a diet rich in fruits, vegetables and plant foods in
reducing the occurrence of human cancer at a number of different sites,
including cancers of the stomach, lung, breast, colon and other epithelial
tumors. Therefore considerable research has focused on identifying
anti-tumor promoting plant-based dietary components. Among the components
with chemopreventive promise, plant phenolics represent a fertile field for
evaluating the potential of dietary substances which can serve as effective
Our research will focus on flavonoids which are known to inhibit protein
kinase C (PKC), the cellular receptor for the phorbol ester tumor promoter,
TPA, a free radical generator and inhibitor of the anti-oxidant defense
system in promotion-sensitive murine epidermal JB6 cells. More
specifically, we will focus on quercetin (QU), which inhibits PKC activity,
and its structural derivatives rutin (RU) and taxifolin (TX), which do no
inhibit PKC activity. Since QU or a PKC inhibitor blocked TPA-induced
transformation of JB6 cells, we wish to determine whether or not the
anti-promoting effects of QU is mediated by PKC. The effect of RU and TX on
TPA-induced transformation and PKC activity in JB6 cells. We will
accomplish our goals by performing anchorage-independent growth assays to
measure transformation and kinase assays to measure PKC activity using
isoform-specific PKC reagents. These investigations into the mechanisms
whereby flavonoids inhibit the rate-limiting tumor promotion step of
carcinogenesis could lead to rational design of novel chemopreventives for
epithelially-derived cancers which account for approximately 90 percent of
cancer deaths in the US.
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