6533b7d3fe1ef96bd1260273

RESEARCH PRODUCT

Resveratrol, a chemopreventive agent, disrupts the cell cycle control of human SW480 colorectal tumor cells

Patricia Passilly-degraceMustapha Cherkaoui MalkiNorbert LatruffeBrigitte JanninDominique Delmas

subject

DNA Replicationendocrine system diseasesCellCyclin AAdenocarcinomaCyclin BProtein Serine-Threonine KinasesResveratrolS Phasechemistry.chemical_compoundCDC2 Protein KinaseStilbenesCDC2-CDC28 KinasesTumor Cells CulturedGeneticsmedicineAnticarcinogenic AgentsHumansCyclin B1Phosphorylationskin and connective tissue diseasesCyclinCyclin-dependent kinase 1biologyKinaseCell growthorganic chemicalsCell CycleCyclin-Dependent Kinase 2Cyclin-dependent kinase 2food and beveragesGeneral MedicineCell cycleFlow CytometryCyclin-Dependent KinasesGrowth InhibitorsNeoplasm ProteinsGene Expression Regulation Neoplasticmedicine.anatomical_structureBiochemistrychemistryResveratrolEnzyme Inductionbiology.proteinCancer researchColorectal NeoplasmsProtein Processing Post-TranslationalCell Division

description

Resveratrol is a natural polyphenolic compound produced by a number of plants and found in high amount in peanuts, seeds, grapes or berries as source of human nutrition. Epidemiological studies strongly suggest that resveratrol may act as a cancer chemopreventive compound. The mechanism by which resveratrol inhibits cell proliferation was studied in human colorectal tumor SW480 cell line. The results show that resveratrol strongly inhibits cell proliferation at the micromolar range in a time- and dose-dependent manner. Resveratrol appears to block the cell cycle at the transition --> G2/M since inhibition of [(3)H]-thymidine incorporation is not observed, while there is an increase of the cell number in S phase. During this inhibition process, resveratrol increases the content of cyclins A and B1 as well as cyclin-dependent kinases Cdk1 and Cdk2. Moreover, resveratrol promotes Cdk1 phosphorylation. In conclusion, resveratrol exerts a strong inhibition of SW480 human colorectal tumor cell proliferation at least by modulating cyclin and cyclin-dependent kinase activities.

https://doi.org/10.3892/ijmm.10.2.193