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Know How Quercetin Helps In Cancer Treatment

Know How Quercetin Helps In Cancer Treatment

Quercetin is one of the most commonly found phytochemicals in foods consumed daily. This polyphenol compound can be found widely in nuts, teas, vegetables, herbs, and usually daily diets.Quercetinhelps in preventing several types of cancers.Quercetinhas an extended range of pharmacological applications, including antioxidant, anti-diabetic, anti-inflammatory, and anti-proliferative roles.

Quercetin acts as the bestCancer Treatmentif earlyColon CancerSymptoms,Breast CancerSymptoms,and Cervical Cancersymptoms are disclosed. The high capability ofQuercetinin free radical scavenging and binding to transition metal ions is due to the presence of two antioxidant pharmacophores in its structure.

Know How Quercetin Helps In Cancer Treatment

Also Read: QUERCETIN

Quercetin is considered necessary in treating different types of cancers due to its possible beneficial effects on human health; antiviral, anti-allergic, antiplatelet, anti-inflammatory, antitumor, and antioxidant activities have been recorded.

Quercetin as agent for chemoprevention

  • Quercetin, like most flavonoids, has potential beneficial effects on health promotion and prevention of diseases, including types of cancers and tumours. The mechanism by whichQuercetinexercises an anti-inflammatory, pro-apoptotic, and chemopreventive role has not yet been fully understood. Still, several models have been presented that attempt to explain its molecular behaviour.
  • One of these models relates toQuercetininhibition of the nuclear factor- kappa B (NF- kappa B), also via the PI3K / Akt / IKK / NF-kappa B signalling axis. Flavonoids, as is widely acknowledged, are naturally occurring inhibitors of NF-kappa B.
  • Quercetin helps in dealing with several types of cancers, such as breast cancer, colon cancer,Prostate CancerandSkin Cancerand is also related to direct or indirect action towards these molecular participants that leads to cancerogenesis.
  • FlavonoidQuercetinis capable of curbing the PI3K / Akt / IKK - alpha/NF- kappa B pathway in human salivary adenoid cystic carcinoma leading to cell apoptosis induction by mitochondrial-dependent mechanisms.
  • Quercetin can inhibit many other kinases and enzymes in addition to PI3K and NF-kappa B. The flavonol may also act positively on kinase/suppressor factors, thus inducing indirect inhibition of kinase.
  • Quercetin is helpful forCancer Treatmentas it increases the oncosuppressor and thus enhances the inhibitory effect on PI3 K function.Quercetin-induced p21 CDK inhibitor with concomitant reduction of pRb phosphorylation, which inhibits the progression of the G1/S cell cycle by trapping E2F1.
  • Akt has a well-documented pro-survival function. Akt's kinase activity is elicited through the signalling pathways for phosphoinositide-3-OH kinase (PI3K), and PI3K-dependent kinase 1/2 (PDK 1/2): inhibition at this stage may, therefore, lead to Akt being inactivated.
  • Quercetin acts as a cancer care provider as it has cell survival inhibition ability. Cancerogenesis and tumour growth, as well as apoptosis induction, are related to upstream PI3 K inactivation becauseQuercetinis a direct antagonist of PI3 K.

Role of Quercetin

What's the primary role ofQuercetinin this articulated network of protein-to-protein cross-talks?

  • Due to its antioxidant, antitumor, and anti-inflammatory activity,Quercetinhas been studied extensively as a chemoprevention agent in several cancer models [Hertog et al., 1993].Quercetinhas been shown to inhibit the proliferation of a wide range of cancers, such as prostate, cervical, lung, breast, and colon.
  • NF-kappa B may induce Anti-apoptotic genes that antagonize the pro-apoptotic function of p53. In this context, the role of p53 is highly complex, and it is probably early to indicate p53 as a good target for Quercetin in the fight against tumours. BCL-3 may also induce the expression of HDM2 and reduce p53 protein levels. There may be a competition between p53 and RelA for binding to mutual coactivator proteins, such as cyclic-AMP sensitive element-binding (CREB)-binding protein (CBP) or p300; on the contrary, there have also been reports of cooperative pathways between p53 and NF- kappa B.
  • Quercetin induces apoptosis in humanCervical Cancer(HeLa) cells by promoting p53 activity and inhibiting NF- kappa B:Quercetininduced p53/p21 mediated cell cycle arrest in G2/M, a result which confirmed previously reported evidence in other tumours. GSK-3 is a crucial regulator of NF- kappa B function, as its inhibition may be approached to combat certain cancers with constitutively active NF- kappa B.
  • The exploration of the role of plant-derived products from dietary intake in the sense of molecular apoptosis control will contribute to a potential understanding of their function in animal cells. It may induce apoptosis as a phytoestrogen either through extrinsic or intrinsic pathways involving NF- kappa B and PI3K / Akt signalling pathways.

Know How Quercetin Helps In Cancer Treatment

Also Read: Anti Cancer Supplements

In conclusion, although a large stack of evidence and theories is still being gathered, many more observations are required due to the increasing number of polyphenolic compounds that reach and invade many research areas with optimistic expectations. Many plant-derived molecules, commonly present in the daily diet of humans, are proving feasible tools in combating tumours by inhibiting the growth of cancer cells with the ability to act as chemopreventive compounds. The goal is to find an appropriate target to treat possible natural compounds, either in food extracts or as real cancer medicines.

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Reference:

  1. Jeong JH, An JY, Kwon YT, Rhee JG, Lee YJ. Effects of low dose quercetin: cancer cell-specific inhibition of cell cycle progression. J Cell Biochem. 2009 Jan 1;106(1):73-82. doi: 10.1002/jcb.21977. PMID: 19009557; PMCID: PMC2736626.
  2. Jana N, B?etislav G, Pavel S, Pavla U. Potential of the Flavonoid Quercetin to Prevent and Treat Cancer - Current Status of Research. Klin Onkol. 2018 Spring;31(3):184-190. English. doi: 10.14735/amko2018184. PMID: 30441971.
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