This page is under construction.
Quercetin is a flavonoid widely distributed in nature. The name has been used since 1857, and is derived from quercetum
(oak forest), after Quercus. It is a naturally occurring polar auxin transport inhibitor. Quercetin is one of the most
abundant dietary flavonoids, with an average daily consumption of 25–50 milligrams.
Several molecules present in the diet, including flavonoids, can inhibit the growth of cancer cells with an ability to act
as “chemopreventers”. Their cancer-preventive effects have been attributed to various mechanisms, including the induction
of cell-cycle arrest and/or apoptosis as well as the antioxidant functions. The antioxidant activity of chemopreventers has
recently received a great interest, essentially because oxidative stress participates in the initiation and progression of
different pathological conditions, including cancer. Since antioxidants are capable of preventing oxidative damage, the wide
use of natural food-derived antioxidants is receiving greater attention as potential anti-carcinogens. Among flavonoids,
quercetin (Qu) is considered an excellent free-radical scavenging antioxidant, even if such an activity strongly depends on
the intracellular availability of reduced glutathione. Apart from antioxidant activity, Quercentine also exerts a direct,
pro-apoptotic effect in tumor cells, and can indeed block the growth of several human cancer cell lines at different phases
of the cell cycle. Both these effects have been documented in a wide variety of cellular models as well as in animal models.
The high toxicity exerted by Qu on cancer cells perfectly matches with the almost total absence of any damages for normal,
non-transformed cells. In this review we discuss the molecular mechanisms that are based on the biological effects of
Quercentine, and their relevance for human health.
How Quercentine might help
Quercetin is a unique dietary polyphenol because it can exert biphasic dose-responses on cells depending on its
concentration. Cancer preventative effects of quercetin are observed at concentrations of approximately 1–40 µM
and are likely mediated by quercetin's antioxidant properties. Pro-oxidant effects are present at cellular
concentrations of 40–100 µM. However, at higher concentrations, many novel pathways in addition to ROS contribute
to its effects. The potent bioactivity of quercetin has led to vigorous study of this compound and revealed numerous
pathways that could interact synergistically to prevent or treat cancer.
Increased consumption of fruits and vegetables can represent an easy strategy to significantly reduce the incidence
of cancer. From this observation, derived mostly from epidemiological data, the new field of chemoprevention has
emerged in the primary and secondary prevention of cancer. Chemoprevention is defined as the use of natural or synthetic
compounds able to stop, reverse, or delay the process of tumorigenesis in its early stages. A large number of
phytochemicals are potentially capable of simultaneously inhibiting and modulating several key factors regulating cell
proliferation in cancer cells. Quercetin is a flavonoid possessing potential chemopreventive properties. It is a
functionally pleiotropic molecule, possessing multiple intracellular targets, affecting different cell signaling processes
usually altered in cancer cells, with limited toxicity on normal cells. Simultaneously targeting multiple pathways may
help to kill malignant cells and slow down the onset of drug resistance. Among the different substrates triggered by
quercetin, we have reviewed the ability of the molecule to inhibit protein kinases involved in deregulated cell growth
in cancer cells.
Quercetin has been detected in significant amounts in green vegetables, citrus fruits and red grape wines. Beneficial
effects attributed to these compounds include anti-inflammatory, antiviral and antitumor properties. The effect of
resveratrol and quercetin on growth of human oral cancer cells is unknown. Resveratrol and quercetin, in concentrations
of 1 to 100 microM, were incubated in triplicates with human oral squamous carcinoma cells SCC-25 in DMEM-HAM's F-12
supplemented with fetal calf serum and antibiotics in an atmosphere of 5% CO2 in air at 37 degrees C for 72 h. Cell
growth was determined by counting the number of viable cells with a hemocytometer. Cell proliferation was measured by
means of incorporation of [3H]thymidine in nuclear DNA. Resveratrol at 10 and 100 microM induced significant
dose-dependent inhibition in cell growth as well as in DNA synthesis. Quercetin exhibited a biphasic effect,
stimulation at 1 and 10 microM, and minimal inhibition at 100 microM in cell growth and DNA synthesis.
Combining 50 microM of resveratrol with 10, 25 and 50 microM of quercetin resulted in a gradual and significant
increase in the inhibitory effect of quercetin on cell growth and DNA synthesis. We conclude that resveratrol or a
combination of resveratrol and quercetin, in concentrations equivalent to that present in red wines, are effective
inhibitors of oral squamous carcinoma cell (SCC-25) growth and proliferation, and warrant further investigation as
cancer chemopreventive agents.