Document Detail

Staurosporine-induced apoptosis is independent of p16 and p21 and achieved via arrest at G2/M and at G1 in U251MG human glioma cell line.
MedLine Citation:
PMID:  12721754     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: The mechanisms involved in the cell cycle and cell death remain unresolved despite much investigation. Staurosporine induces cell death and G1 or G2/M arrest in a dose-dependent manner, but the mechanisms remain unknown. METHODS: In the present study an adenovirus vector expressing p16 or p21 genes in human glioma cell lines was used to examine cell cycle regulation and cell death induced by staurosporine. RESULTS: A low concentration (</=10 n M) of staurosporine induced G1 arrest of U251MG cells, whereas a high concentration (>/=30 n M) induced G2/M arrest and finally induced apoptosis via a caspase-3-activated pathway from both the G2/M and G1 phases. However, pRb was dephosphorylated and cdc2 was inhibited at both the low and the high concentrations of staurosporine, indicating that the mechanisms of cell cycle regulation are not simply p53-Rb- or cdc2-dependent pathways. CONCLUSIONS: Forced G1 arrest by transfection with p16 or p21 genes did not alter the rate of staurosporine-induced cell death. This implies that an unknown pathway of apoptosis occurs from the G1 phase.
Fumiyuki Yamasaki; Seiji Hama; Hiroyuki Yoshioka; Yoshinori Kajiwara; Kaita Yahara; Kazuhiko Sugiyama; Yuji Heike; Kazunori Arita; Kaoru Kurisu
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Publication Detail:
Type:  Journal Article     Date:  2003-03-20
Journal Detail:
Title:  Cancer chemotherapy and pharmacology     Volume:  51     ISSN:  0344-5704     ISO Abbreviation:  Cancer Chemother. Pharmacol.     Publication Date:  2003 Apr 
Date Detail:
Created Date:  2003-04-30     Completed Date:  2003-06-27     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  7806519     Medline TA:  Cancer Chemother Pharmacol     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  271-83     Citation Subset:  IM    
Department of Neurosurgery, Faculty of Medicine, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima, Japan.
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MeSH Terms
Antineoplastic Agents / pharmacology*
Apoptosis / drug effects*,  genetics
Brain Neoplasms / genetics*,  pathology
CDC2 Protein Kinase / biosynthesis
Cell Cycle / drug effects*,  genetics
Cell Cycle Proteins / genetics*
Cyclin-Dependent Kinase Inhibitor p16 / genetics
Cyclin-Dependent Kinase Inhibitor p21
Cyclins / genetics
Dose-Response Relationship, Drug
G1 Phase / drug effects,  genetics
G2 Phase / drug effects,  genetics
Gene Expression Regulation, Neoplastic / drug effects,  genetics
Genetic Vectors
Glioma / genetics*,  pathology
Retinoblastoma Protein / biosynthesis
Staurosporine / pharmacology*
Tumor Cells, Cultured
Reg. No./Substance:
0/Antineoplastic Agents; 0/CDKN1A protein, human; 0/Cell Cycle Proteins; 0/Cyclin-Dependent Kinase Inhibitor p16; 0/Cyclin-Dependent Kinase Inhibitor p21; 0/Cyclins; 0/Retinoblastoma Protein; 62996-74-1/Staurosporine; EC Protein Kinase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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