Limits...
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.


Anticancer pathways and mechanisms of quercetin.
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC5037516&req=5

nutrients-08-00529-f003: Anticancer pathways and mechanisms of quercetin.

Mentions: Quercetin has the ability to actively inhibit the JAK-STAT signaling pathway in various inflammatory disorders. Furthermore, treatment of activated T cells with quercetin in vitro inhibited the interleukin-12 (IL-12)-induced phosphorylation of JAK2, tyrosine kinase-2 (TYK2), STAT3, and STAT4, which result in decreased levels of T cell propagation and Th1 variation [67]. Therefore, these anti-inflammatory and antiapoptotic properties of quercetin have a key role in the reduction of cancer by controlling the toll-like receptor-2 (TLR2) and JAK2/STAT3 pathway and causing the inhibition of STAT3 tyrosine phosphorylation within inflammatory cells [68]. Pretreatment of cholangiocarcinoma cells with quercetin inhibited the cytokine-mediated upregulation of inducible nitric oxide synthase (iNOS) and expression of intercellular adhesion molecule-1 (ICAM-1) in the JAK/STAT cascade pathway. Also, quercetin blocked the activation of inflammatory cytokine interleukin-6 and interferon-γ [69]. It was reported that LPS-induced STAT1 activation was inhibited by quercetin in combination with its profound inhibitory effects on iNOS and NF-κB expression, which are persistently involved in activation of interleukin-2 (IL-2) as shown in Figure 3 [70].


Molecular Targets Underlying the Anticancer Effects of Quercetin: An Update
Anticancer pathways and mechanisms of quercetin.
© Copyright Policy
Related In: Results  -  Collection

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

nutrients-08-00529-f003: Anticancer pathways and mechanisms of quercetin.
Mentions: Quercetin has the ability to actively inhibit the JAK-STAT signaling pathway in various inflammatory disorders. Furthermore, treatment of activated T cells with quercetin in vitro inhibited the interleukin-12 (IL-12)-induced phosphorylation of JAK2, tyrosine kinase-2 (TYK2), STAT3, and STAT4, which result in decreased levels of T cell propagation and Th1 variation [67]. Therefore, these anti-inflammatory and antiapoptotic properties of quercetin have a key role in the reduction of cancer by controlling the toll-like receptor-2 (TLR2) and JAK2/STAT3 pathway and causing the inhibition of STAT3 tyrosine phosphorylation within inflammatory cells [68]. Pretreatment of cholangiocarcinoma cells with quercetin inhibited the cytokine-mediated upregulation of inducible nitric oxide synthase (iNOS) and expression of intercellular adhesion molecule-1 (ICAM-1) in the JAK/STAT cascade pathway. Also, quercetin blocked the activation of inflammatory cytokine interleukin-6 and interferon-γ [69]. It was reported that LPS-induced STAT1 activation was inhibited by quercetin in combination with its profound inhibitory effects on iNOS and NF-κB expression, which are persistently involved in activation of interleukin-2 (IL-2) as shown in Figure 3 [70].

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.