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Molecular Targets Underlying the Anticancer Effects of Quercetin: An Update

View Article: PubMed Central - PubMed

ABSTRACT

Quercetin, a medicinally important member of the flavonoid family, is one of the most prominent dietary antioxidants. It is present in a variety of foods—including fruits, vegetables, tea, wine, as well as other dietary supplements—and is responsible for various health benefits. Numerous pharmacological effects of quercetin include protection against diseases, such as osteoporosis, certain forms of malignant tumors, and pulmonary and cardiovascular disorders. Quercetin has the special ability of scavenging highly reactive species, such as hydrogen peroxide, superoxide anion, and hydroxyl radicals. These oxygen radicals are called reactive oxygen species, which can cause oxidative damage to cellular components, such as proteins, lipids, and deoxyribonucleic acid. Various oxygen radicals play important roles in pathophysiological and degenerative processes, such as aging. Subsequently, several studies have been performed to evaluate possible advantageous health effects of quercetin and to collect scientific evidence for these beneficial health claims. These studies also gather data in order to evaluate the exact mechanism(s) of action and toxicological effects of quercetin. The purpose of this review is to present and critically analyze molecular pathways underlying the anticancer effects of quercetin. Current limitations and future directions of research on this bioactive dietary polyphenol are also critically discussed.

No MeSH data available.


Related in: MedlinePlus

Modulation of mitochondrial apoptotic signaling pathways by quercetin. Quercetin induces p53 activation resulting in upregulation of Bax and downregulation of Bcl-2 in tumor cells. This leads to caspase activation and ultimately apoptotic cell death.
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nutrients-08-00529-f004: Modulation of mitochondrial apoptotic signaling pathways by quercetin. Quercetin induces p53 activation resulting in upregulation of Bax and downregulation of Bcl-2 in tumor cells. This leads to caspase activation and ultimately apoptotic cell death.

Mentions: There are various reports which document modulatory effects of quercetin and other flavonoids on signal transduction pathways. The use of quercetin enhances the cell death process in HepG2 human hepatoma cells. There are two mechanisms involved in this process; one is the activation of caspase-3 and caspase-9, but not caspase-8. The other mechanism involves an increase in the translocation of proapoptotic Bax to the membrane of mitochondria [112]. In a similar study, it has been shown that quercetin causes the cleavage of polymerase and also potentiates the upregulation of Bax (Figure 4). Quercetin decreases the levels of key oncogenic protein Ras in cancer cells and blocks the cell proliferation and survival [113].


Molecular Targets Underlying the Anticancer Effects of Quercetin: An Update
Modulation of mitochondrial apoptotic signaling pathways by quercetin. Quercetin induces p53 activation resulting in upregulation of Bax and downregulation of Bcl-2 in tumor cells. This leads to caspase activation and ultimately apoptotic cell death.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5037516&req=5

nutrients-08-00529-f004: Modulation of mitochondrial apoptotic signaling pathways by quercetin. Quercetin induces p53 activation resulting in upregulation of Bax and downregulation of Bcl-2 in tumor cells. This leads to caspase activation and ultimately apoptotic cell death.
Mentions: There are various reports which document modulatory effects of quercetin and other flavonoids on signal transduction pathways. The use of quercetin enhances the cell death process in HepG2 human hepatoma cells. There are two mechanisms involved in this process; one is the activation of caspase-3 and caspase-9, but not caspase-8. The other mechanism involves an increase in the translocation of proapoptotic Bax to the membrane of mitochondria [112]. In a similar study, it has been shown that quercetin causes the cleavage of polymerase and also potentiates the upregulation of Bax (Figure 4). Quercetin decreases the levels of key oncogenic protein Ras in cancer cells and blocks the cell proliferation and survival [113].

View Article: PubMed Central - PubMed

ABSTRACT

Quercetin, a medicinally important member of the flavonoid family, is one of the most prominent dietary antioxidants. It is present in a variety of foods—including fruits, vegetables, tea, wine, as well as other dietary supplements—and is responsible for various health benefits. Numerous pharmacological effects of quercetin include protection against diseases, such as osteoporosis, certain forms of malignant tumors, and pulmonary and cardiovascular disorders. Quercetin has the special ability of scavenging highly reactive species, such as hydrogen peroxide, superoxide anion, and hydroxyl radicals. These oxygen radicals are called reactive oxygen species, which can cause oxidative damage to cellular components, such as proteins, lipids, and deoxyribonucleic acid. Various oxygen radicals play important roles in pathophysiological and degenerative processes, such as aging. Subsequently, several studies have been performed to evaluate possible advantageous health effects of quercetin and to collect scientific evidence for these beneficial health claims. These studies also gather data in order to evaluate the exact mechanism(s) of action and toxicological effects of quercetin. The purpose of this review is to present and critically analyze molecular pathways underlying the anticancer effects of quercetin. Current limitations and future directions of research on this bioactive dietary polyphenol are also critically discussed.

No MeSH data available.


Related in: MedlinePlus