Effects of structurally related flavonoids on cell cycle progression of human melanoma cells: regulation of cyclin-dependent kinases CDK2 and CDK111Abbreviations: CDK, cyclin-dependent kinase; CKI, CDK inhibitor; PI 3-kinase, phosphatidylinositol 3-kinase; PKC, protein kinase C; DTT, dithiothreitol; RIPA, radioimmunoprecipitation assay buffer.

Casagrande, Fabrice; Darbon, Jean‐Marie

doi:10.1016/s0006-2952(01)00583-4

Cited by 273 publications

(59 citation statements)

References 39 publications

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“…Within the flavonoid family, quercetin is the most potent scavenger of ROS, including O 2 d- (Hanasaki et al 1994;Cushnie and Lamb 2005). This natural phenolic compound potently inhibits melanoma cell proliferation by inhibiting PI 3-kinase and the protein kinase CDK2 (Casagrande and Darbon 2001). It should be noted, however, that quercetin also shows paradoxal actions in neuronal cells.…”

Section: Discussionmentioning

confidence: 99%

“…Quercetin is a flavonoid compound possessing free radical scavenging properties and may protect from oxidative injury by its ability to modulate intracellular signals and promote cellular survival (Mercer et al 2005). Like resveratrol, it has cardioprotective (Brookes et al 2002), anticarcinogenic (Casagrande and Darbon 2001;Lee et al 2008), antioxidant (Heo and Lee 2004), and antiapoptotic (Formica and Regelson 1995) properties. Recent reports show that quercetin, when used at relative high doses, does not protect against H 2 O 2 -induced cell death in undifferentiated PC12 cells (Sasaki et al 2007) and may induce apoptosis in primary neuronal cultures (Jakubowicz-Gil et al 2008a).…”

Section: Introductionmentioning

confidence: 99%

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Protective Effects of Resveratrol and Quercetin Against MPP+ -Induced Oxidative Stress Act by Modulating Markers of Apoptotic Death in Dopaminergic Neurons

2009

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Reactive oxygen species produced by oxidative stress may participate in the apoptotic death of dopamine neurons distinctive of Parkinson's disease. Resveratrol, a red wine extract, and quercetin, found mainly in green tea, are two natural polyphenols, presenting antioxidant properties in a variety of cellular paradigms. The aim of this study was to evaluate the effect of resveratrol and quercetin on the apoptotic cascade induced by the administration of 1-methyl-4-phenylpyridinium ion (MPP(+)), a Parkinsonian toxin, provoking the selective degeneration of dopaminergic neurons. Our results show that a pre-treatment for 3 h with resveratrol or quercetin before MPP(+) administration could greatly reduce apoptotic neuronal PC12 death induced by MPP(+). We also demonstrated that resveratrol or quercetin modulates mRNA levels and protein expression of Bax, a pro-apoptotic gene, and Bcl-2, an anti-apoptotic gene. We then evaluated the release of cytochrome c and the nuclear translocation of the apoptosis-inducing factor (AIF). Altogether, our results indicate that resveratrol and quercetin diminish apoptotic neuronal cell death by acting on the expression of pro- and anti-apoptotic genes. These findings support the role of these natural polyphenols in preventive and/or complementary therapies for several human neurodegenerative diseases caused by oxidative stress and apoptosis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Protective Effects of Resveratrol and Quercetin Against MPP+ -Induced Oxidative Stress Act by Modulating Markers of Apoptotic Death in Dopaminergic Neurons

2009

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“…Recently, genistein was shown to increase Wee1 kinase and phosphorylation of CDC2 resulting in inhibition of CDC2 kinase activity and an induction of G2/M arrest in HepG2 hepatoma cells [80]. Recently, many studies have reported G2/M arrest inducing effect of many natural flavonoids such as casticin (from Viticis fructus) in KB cells [81], isoliquiritigenin (from licorice) in lung cancer A549 and prostate cancer DU145 and LNCaP cells [82,83], apigenin in colon carcinoma SW480, HT-29 and MG63, and breast carcinoma MCF-7 and MDA-MB-468 cells [84][85][86], kaempferol in melanoma OCM-1 and colon carcinoma SW480 cells [84,87], and luteolin and quercetin in SW480 cells [84]. CDC25C and CDC2 are also known to be sequestered by 14-3-3 protein in cytoplasm, and therefore, remain inactive [88].…”

Section: Flavonoids Targeting Cdc25c-cdc2-cyclin B1 Regulationmentioning

confidence: 99%

Natural Flavonoids Targeting Deregulated Cell Cycle Progression in Cancer Cells

Singh¹,

Agarwal²

2006

CDT

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The prolonged duration requiring alteration of multi-genetic and epigenetic molecular events for cancer development provides a strong rationale for cancer prevention, which is developing as a potential strategy to arrest or reverse carcinogenic changes before the appearance of the malignant disease. Cell cycle progression is an important biological event having controlled regulation in normal cells, which almost universally becomes aberrant or deregulated in transformed and neoplastic cells. In this regard, targeting deregulated cell cycle progression and its modulation by various natural and synthetic agents are gaining widespread attention in recent years to control the unchecked growth and proliferation in cancer cells. In fact, a vast number of experimental studies convincingly show that many phytochemicals halt uncontrolled cell cycle progression in cancer cells. Among these phytochemicals, natural flavonoids have been identified as a one of the major classes of natural anticancer agents exerting antineoplastic activity via cell cycle arrest as a major mechanism in various types of cancer cells. This review is focused at the modulatory effects of natural flavonoids on cell cycle regulators including cyclin-dependent kinases and their inhibitors, cyclins, p53, retinoblastoma family of proteins, E2Fs, check-point kinases, ATM/ATR and survivin controlling G1/S and G2/M check-point transitions in cell cycle progression, and discusses how these molecular changes could contribute to the antineoplastic effects of natural flavonoids.

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“…The cytotoxic activity of flavonoids involves the inhibition of several molecular targets and pathways: DNA topoisomerases I and II [64], cyclin-dependent kinases CDK2 and/or CDK1 [65], androgen receptor signaling [66], actin polymerization [67,68], activation of p53, and inhibition of NFkB pathways [69]. Flavonoids activate the caspase-mediated signal transduction pathways, consecutively stimulating the tumor-suppressor protein p53, which consequently triggers cell apoptosis [69].…”

Section: Anticancer Activity Of Flavonoids Metal Complexesmentioning

confidence: 99%

Flavonoid Complexes as Promising Anticancer Metallodrugs

Uivaroşi¹,

Arbănași²

2017

Flavonoids - From Biosynthesis to Human Health

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Flavonoid metal complexes commonly exhibit an improvement of biological activity compared to the parent ligands. This chapter is focused on the antioxidant and anticanccer properties of flavonoid metal complexes, in correlation with their binding ability to vital macromolecules such as nucleic acids and serum proteins. Perspectives for an adequate formulation of these complexes were also discussed.

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Cited by 273 publications

References 39 publications

Protective Effects of Resveratrol and Quercetin Against MPP+ -Induced Oxidative Stress Act by Modulating Markers of Apoptotic Death in Dopaminergic Neurons

Protective Effects of Resveratrol and Quercetin Against MPP+ -Induced Oxidative Stress Act by Modulating Markers of Apoptotic Death in Dopaminergic Neurons

Natural Flavonoids Targeting Deregulated Cell Cycle Progression in Cancer Cells

Flavonoid Complexes as Promising Anticancer Metallodrugs

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