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Titolo:
Decreased cyclin B1 expression contributes to G(2) delay in human brain tumor cells after treatment with camptothecin
Autore:
Janss, AJ; Maity, A; Tang, CB; Muschel, RJ; McKenna, WG; Sutton, L; Phillips, PC;
Indirizzi:
Childrens Hosp Philadelphia, Div Neurol, Philadelphia, PA 19104 USA Childrens Hosp Philadelphia Philadelphia PA USA 19104 lphia, PA 19104 USA Childrens Hosp Philadelphia, Div Oncol, Philadelphia, PA 19104 USA Childrens Hosp Philadelphia Philadelphia PA USA 19104 lphia, PA 19104 USA Childrens Hosp Philadelphia, Div Neurosurg, Philadelphia, PA 19104 USA Childrens Hosp Philadelphia Philadelphia PA USA 19104 lphia, PA 19104 USA Univ Penn, Sch Med, Dept Radiat Oncol, Philadelphia, PA 19104 USA Univ Penn Philadelphia PA USA 19104 iat Oncol, Philadelphia, PA 19104 USA Univ Penn, Sch Med, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA UnivPenn Philadelphia PA USA 19104 & Lab Med, Philadelphia, PA 19104 USA
Titolo Testata:
NEURO-ONCOLOGY
fascicolo: 1, volume: 3, anno: 2001,
pagine: 11 - 21
SICI:
1522-8517(200101)3:1<11:DCBECT>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
CENTRAL-NERVOUS-SYSTEM; HAMSTER OVARY CELLS; PROTEIN-KINASE; HELA-CELLS; DNA-DAMAGE; TRANSPLANTABLE XENOGRAFTS; ALKYLATING-AGENTS; NITROGEN-MUSTARD; P34CDC2 KINASE; MESSENGER-RNA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
56
Recensione:
Indirizzi per estratti:
Indirizzo: Janss, AJ Childrens Hosp Philadelphia, Div Neurol, 324 S 34th St, Philadelphia, PA 19104 USA Childrens Hosp Philadelphia 324 S 34th St Philadelphia PA USA 19104
Citazione:
A.J. Janss et al., "Decreased cyclin B1 expression contributes to G(2) delay in human brain tumor cells after treatment with camptothecin", NEURO-ONCOL, 3(1), 2001, pp. 11-21

Abstract

DNA damage produces delayed mitosis (G(2)/M delay) in proliferating cells,and shortening the delay sensitizes human malignant glioma and medulloblastoma cells to cytotoxic chemotherapy. Although activation of the cyclin-dependent kinase CDC2 mediates G(2)/M transition in all tumor cells studied todate, regulation of CDC2 varies between tumor types. Persistent hyperphosphorylation of kinase and reduced cyclin expression have been implicated as mediators of treatment-induced G(2) delay in different tumor models. To evaluate regulation of G(2)/M transition in human brain tumors, we studied theexpression and/or activity of CDC2 kinase and cyclins A and B1 in U-251 MGand DAOY medulloblastoma cells after their treatment with camptothecin (CPT). Synchronized cells were treated during S phase, then harvested at predetermined intervals for evaluation of cell cycle kinetics, kinase activity mRNA, and protein expression. CPT produced G(2) delay associated with decreased CDC2 kinase activity and cyclin B1 expression. Kinase activity was associated with CDC2 bound to cyclin B1, not cyclin A, in both cell lines. Cyclin A mRNA and protein expression were reduced after CPT treatment; however,decreased protein expression was short lived and moderate in the glioma and primitive neuroectodermal tumor/medulloblastoma cells, respectively. We conclude that G(2) delay is a common response of brain tumor cells to chemotherapy with topoisomerase I inhibitors and that a mechanism of this delay may he reduced expression of cyclin B1.

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Documento generato il 26/01/20 alle ore 16:02:40