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dc.contributor.authorThomas, C. G.en
dc.contributor.authorVezyraki, P. E.en
dc.contributor.authorKalfakakou, V. P.en
dc.contributor.authorEvangelou, A. M.en
dc.rightsDefault Licence-
dc.subjectAscorbic Acid/*pharmacologyen
dc.subjectCell Cycle/*drug effectsen
dc.subjectCell Cycle Proteins/*metabolismen
dc.subjectCell Line, Tumoren
dc.subjectDNA/antagonists & inhibitors/biosynthesisen
dc.subjectEnzyme Activation/drug effectsen
dc.subjectG2 Phase/*drug effectsen
dc.subjectHeLa Cellsen
dc.subjectMitosis/*drug effectsen
dc.subjectModels, Biologicalen
dc.subjectS Phase/*drug effectsen
dc.subjectcdc25 Phosphatases/*metabolismen
dc.titleVitamin C transiently arrests cancer cell cycle progression in S phase and G2/M boundary by modulating the kinetics of activation and the subcellular localization of Cdc25C phosphataseen
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.abstractRegulation of cell cycle progression involves redox (oxidation-reduction)-dependent modification of proteins including the mitosis-inducing phosphatase Cdc25C. The role of vitamin C (ascorbic acid, ASC), a known modulator of the cellular redox status, in regulating mitotic entry was investigated in this study. We demonstrated that vitamin C inhibits DNA synthesis in HeLa cells and, mainly the form of dehydroascorbic acid (DHA), delays the entry of p53-deficient synchronized HeLa and T98G cancer cells into mitosis. High concentrations of Vitamin C caused transient S and G2 arrest in both cell lines by delaying the activation of the M-phase promoting factor (MPF), Cdc2/cyclin-B complex. Although vitamin C did not inhibit the accumulation of cyclin-B1, it may have increased the level of Cdc2 inhibitory phosphorylation. This was achieved by transiently maintaining Cdc25C, the activator of Cdc2, both in low levels and in a phosphorylated on Ser216 inactive form that binds to 14-3-3 proteins contributing thus to the nuclear exclusion of Cdc25C. As expected, vitamin C prevented the nuclear accumulation of Cdc25C in both cell lines. In conclusion, it seems that vitamin C induces transient cell cycle arrest, at least in part, by delaying the accumulation and the activation of Cdc25C.en
heal.journalNameJ Cell Physiolen
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