Vitamin 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 phosphatase
| dc.contributor.author | Thomas, C. G. | en |
| dc.contributor.author | Vezyraki, P. E. | en |
| dc.contributor.author | Kalfakakou, V. P. | en |
| dc.contributor.author | Evangelou, A. M. | en |
| dc.date.accessioned | 2015-11-24T19:41:58Z | |
| dc.date.available | 2015-11-24T19:41:58Z | |
| dc.identifier.issn | 0021-9541 | - |
| dc.identifier.uri | https://olympias.lib.uoi.gr/jspui/handle/123456789/24561 | |
| dc.rights | Default Licence | - |
| dc.subject | Antioxidants/pharmacology | en |
| dc.subject | Ascorbic Acid/*pharmacology | en |
| dc.subject | Cell Cycle/*drug effects | en |
| dc.subject | Cell Cycle Proteins/*metabolism | en |
| dc.subject | Cell Line, Tumor | en |
| dc.subject | DNA/antagonists & inhibitors/biosynthesis | en |
| dc.subject | Enzyme Activation/drug effects | en |
| dc.subject | G2 Phase/*drug effects | en |
| dc.subject | HeLa Cells | en |
| dc.subject | Humans | en |
| dc.subject | Kinetics | en |
| dc.subject | Mitosis/*drug effects | en |
| dc.subject | Models, Biological | en |
| dc.subject | S Phase/*drug effects | en |
| dc.subject | cdc25 Phosphatases/*metabolism | en |
| dc.title | Vitamin 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 phosphatase | en |
| heal.abstract | Regulation 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.access | campus | - |
| heal.fullTextAvailability | TRUE | - |
| heal.identifier.primary | 10.1002/jcp.20405 | - |
| heal.identifier.secondary | http://www.ncbi.nlm.nih.gov/pubmed/15887239 | - |
| heal.identifier.secondary | http://onlinelibrary.wiley.com/store/10.1002/jcp.20405/asset/20405_ftp.pdf?v=1&t=h0c6japx&s=34c2a57cbace42707143596ce9f283f2a7cfacfd | - |
| heal.journalName | J Cell Physiol | en |
| heal.journalType | peer-reviewed | - |
| heal.language | en | - |
| heal.publicationDate | 2005 | - |
| heal.recordProvider | Πανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικής | el |
| heal.type | journalArticle | - |
| heal.type.el | Άρθρο Περιοδικού | el |
| heal.type.en | Journal article | en |
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