Document Detail

G2-phase arrest through p21(WAF1 / Cip1) induction and cdc2 repression by gnidimacrin in human hepatoma HLE cells.
MedLine Citation:
PMID:  19414386     Owner:  NLM     Status:  MEDLINE    
Gnidimacrin (NSC252940) shows significant antiproliferating activity against human tumor cell lines. This compound binds to and directly activates protein kinase C (PKC). Human hepatoma HLE cells, which lose p53 function and retinoblastoma protein (Rb) expression, are resistant to gnidimacrin. However, PKC betaII gene-transfected HLE (HLE/PKC betaII) cells became sensitive to gnidimacrin, through which cdc2 inhibition and G(2)-phase arrest was caused. p21(WAF1/Cip1) induction and cdc2 reduction were observed and this reduction was abolished through the suppression of p21(WAF1/Cip1) induction by the MEK1/2 inhibitor U0126. Translocation of E2F-4 to the nucleus was also observed in the cells but not in parental HLE cells. Consequently gnidimacrin inhibited cell growth through G(2)-phase arrest not only by the p21(WAF1/Cip1)-dependent suppression of cdc2 activity, but also by subsequent transcriptional suppression of cdc2 itself. In addition, involvement of E2F-4 in cdc2 suppression through a long-lasting induction of p21(WAF1/Cip1) by gnidimacrin is suggested in HLE/PKC betaII cells.
Mitsuzi Yoshida; Yuki Matsui; Akira Iizuka; Yoshinori Ikarashi
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Anticancer research     Volume:  29     ISSN:  0250-7005     ISO Abbreviation:  Anticancer Res.     Publication Date:  2009 Apr 
Date Detail:
Created Date:  2009-05-05     Completed Date:  2009-07-02     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8102988     Medline TA:  Anticancer Res     Country:  Greece    
Other Details:
Languages:  eng     Pagination:  1349-54     Citation Subset:  IM    
National Cancer Center Research Institute, Tokyo 104-0045, Japan.
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MeSH Terms
Blotting, Western
Carcinoma, Hepatocellular / drug therapy*,  metabolism,  pathology
Cell Proliferation / drug effects
Cyclin B / genetics,  metabolism*
Cyclin-Dependent Kinase Inhibitor p21 / genetics,  metabolism*
Diterpenes / pharmacology*
Flow Cytometry
G2 Phase / drug effects*
Liver Neoplasms / drug therapy*,  metabolism,  pathology
RNA, Messenger / genetics,  metabolism
Reactive Oxygen Species / metabolism
Reverse Transcriptase Polymerase Chain Reaction
Tumor Cells, Cultured
Reg. No./Substance:
0/CDC2 protein, human; 0/CDKN1A protein, human; 0/Cyclin B; 0/Cyclin-Dependent Kinase Inhibitor p21; 0/Diterpenes; 0/RNA, Messenger; 0/Reactive Oxygen Species; 60796-70-5/gnidimacrin

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