Preventive effect of the flavonoid, quercetin, on hepatic cancer in rats via oxidant/antioxidant activity: molecular and histological evidences

Seufi, AlaaEddeen M.; Ibrahim, Safinz S; El-Maghraby, Tarek K; Hafez, Elsayed E.

doi:10.1186/1756-9966-28-80

Cited by 112 publications

(71 citation statements)

References 25 publications

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“…18,19) In addition to these beneficial effects, quercetin plays preventive and therapeutic roles in various types of cancer and cancer cells. [20][21][22][23][24][25] However, the anticancer effect of quercetin in NSCLC cells has been rarely addressed, and the underlying molecular mechanism remains to be determined.Here, we investigated the growth inhibitory role of quercetin in three NSCLC cell lines and found that its effect is p53-independent and triggered by apoptosis. Subsequent microarray analysis using H460 cells indicated that quercetin enhances the expression of genes associated with death receptor signaling and cell cycle inhibition, but decreases the expression of genes involved in nuclear factor (NF)-κB activation.…”

mentioning

confidence: 99%

Quercetin Potentiates Apoptosis by Inhibiting Nuclear Factor-kappaB Signaling in H460 Lung Cancer Cells

Youn

Jeong

et al. 2013

Biological & Pharmaceutical Bulletin

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The herbal flavonoid quercetin inhibits the growth of various cancer cells, but how it affects human cancer cells, particularly lung cancer cells, is unclear. We investigated the anticancer activity of quercetin and the underlying molecular mechanisms in non-small cell lung cancer (NSCLC) cells. Quercetin strongly inhibited cell proliferation, and increased sub-G1 and apoptotic cell populations regardless of p53 status. Quercetin-induced apoptosis was verified by caspase cleavage, Hoechst staining, trypan blue exclusion, and DNA fragmentation assays. Microarray analysis using H460 cells indicated that quercetin increased the expression of genes associated with death receptor signaling tumor necrosis factor-related apoptosis-inducing ligand receptor (TRAILR), caspase-10, interleukin (IL) 1R DNA fragmentation faotor 45 (DFF45), tumor necrosis factor receptor (TNFR) 1, FAS, inhibitor of kappaBalpha (IκBα)) and cell cycle inhibition growth arrest and DNA-damage inducible 45 (GADD45), p21 Cip1), but decreased the expression of genes involved in nuclear factor (NF)-kappaB activation (NF-κB, IKKα). Further validation assays confirmed that quercetin inhibited growth by suppressing NF-κB and by increasing the expression of death receptors and cell cycle inhibitors. Taken together, these findings suggest that quercetin may be useful in the prevention and therapy of NSCLC.Key words quercetin; lung cancer; apoptosis; death receptor; nuclear factor-kappaB pathway Lung cancer is the leading cause of cancer death in many developed countries because of its poor prognosis. Non-small cell lung cancer (NSCLC) accounts for 85% of lung cancer cases, of which 70% show advanced-stage disease at the time of diagnosis.1,2) Although various chemical drugs have been developed, 3,4) frequent chemoresistance and side effects in patients with NSCLC require the development of new preventive and therapeutic agents. High intake of flavonoids from fruits and vegetables is associated with a low risk of various cancers, 5-10) including lung cancer. 11,12) Of these polyphenolic flavonoids, quercetin is readily found in fruits, vegetables, green and black tea, and various medical plants such as Euonymus alatus (Thunb.) Sieb. Quercetin can act as either an antioxidant or a prooxidant depending on its concentration (1-40 µm or 40-100 µm, respectively). 13,14) Numerous studies have reported a broad range of pharmacological properties of quercetin, including benefits for inflammation, 15) atherosclerosis, 16) hypertension, 17) and neurodegeneration. 18,19) In addition to these beneficial effects, quercetin plays preventive and therapeutic roles in various types of cancer and cancer cells. [20][21][22][23][24][25] However, the anticancer effect of quercetin in NSCLC cells has been rarely addressed, and the underlying molecular mechanism remains to be determined.Here, we investigated the growth inhibitory role of quercetin in three NSCLC cell lines and found that its effect is p53-independent and triggered by apoptosis. Subsequent microarray analysis usin...

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confidence: 99%

Quercetin Potentiates Apoptosis by Inhibiting Nuclear Factor-kappaB Signaling in H460 Lung Cancer Cells

Youn

Jeong

et al. 2013

Biological & Pharmaceutical Bulletin

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“…Quercetin also prevented early stages of azoxymethane induced colorectal carcinogenesis [62]. Further studies showed preventive effects of Quercetin against NDEA induced hepatocellular carcinoma by inhibiting DNA specific mutations [63]. Quercetin protected Caco-2 and Hep G2 cells against H2O2-induced DNA damage [64].…”

Section: Dna Damage Prevention By Flavonoids With Implications To Carmentioning

confidence: 99%

Role of Flavonoids in DNA Damage and Carcinogenesis Prevention

Tiwari¹,

Mishra²

2017

J Carcinog Mutagen

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High level of ionizing radiation and various other mutagenic agents can damage DNA and induce carcinogenesis which may be transferred to offspring's. Flavonoids are major antioxidant compounds obtained from plants and form a significant proportion of most diets. In this review, we have summarized the present understanding of the roles of various flavonoids as preventive approaches against DNA damage and carcinogenesis.

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“…Schistosomiasis) may also contribute to the etiology or progression of the disease [4]. Liver carcinogenesis may also develop through the progressive accumulation of different mutations (genetic) and/or gene products (protein), which eventually lead to malignant transformation [5,6].…”

Section: Introductionmentioning

confidence: 99%

Can methanolic extract of Nigella sativa seed affect glyco-regulatory enzymes in experimental hepatocellular carcinoma?

Abdel-Hamid

Abd-Elghany

Nazmy

et al. 2012

Environ Health Prev Med

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Background and aim To investigate the possible modulating role of ''Nigella sativa'' (NS), a plant commonly used in Egyptian traditional medicine, on premalignant perturbations in three glycol-regulatory enzymes in an experimental rat model of hepatocellular carcinoma (HCC). Methods Thirty-six (36) male albino rats were divided into four groups (n = 9). Group 1 served as a normal control, group 2 was treated with methanolic extract of Nigella sativa (MENS) (1 g/kg/day, orally) for 14 weeks, group 3 received a single intraperitoneal dose of diethyl nitrosamine (DENA) (200 mg/kg), followed 2 weeks later by a subcutaneous injection of carbon tetrachloride (CCl 4 , 3 ml/kg/week/6 weeks) and group IV was treated with MENS for 2 weeks prior to administration of the carcinogenic combination (DENA ? CCl 4 , as in group 3) until the end of the experiment. The total period of the experiment was 14 weeks. Results In the DENA ? CCl 4 -treated group, there was a significant increase in the relative liver weight, serum alpha fetoprotein level and the activities of hexokinase, glyceraldehyde phosphate dehydrogenase and glucose 6 phosphate dehydrogenase in both the serum and liver homogenate; this was accompanied by a subsequent decrease in body weight. Pre-treatment with MENS significantly maintained these parameters close to the normal condition. Conclusion Based on these results, we conclude that MENS has a chemo-preventive effect against the progression into liver malignancy through its modulation of the energy metabolic pathways (i.e. glycolysis) that may be involved in hepatocarcinogenesis.

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Preventive effect of the flavonoid, quercetin, on hepatic cancer in rats via oxidant/antioxidant activity: molecular and histological evidences

Cited by 112 publications

References 25 publications

Quercetin Potentiates Apoptosis by Inhibiting Nuclear Factor-kappaB Signaling in H460 Lung Cancer Cells

Quercetin Potentiates Apoptosis by Inhibiting Nuclear Factor-kappaB Signaling in H460 Lung Cancer Cells

Role of Flavonoids in DNA Damage and Carcinogenesis Prevention

Can methanolic extract of Nigella sativa seed affect glyco-regulatory enzymes in experimental hepatocellular carcinoma?

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