Document Detail


Securinine induces p73-dependent apoptosis preferentially in p53-deficient colon cancer cells.
MedLine Citation:
PMID:  20133503     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The identification of agents that preferentially kill cancer cells while protecting normal cells offers the potential to overcome toxicities found in many existing chemotherapeutic agents. Because p53 is frequently inactivated in cancer, agents that preferentially kill p53-null cells and protect wild-type p53-expressing cells are highly desirable chemotherapeutic agents. By using pairs of isogenic colon cancer cell lines that differ only in p53 expression (RKO and HCT116), securinine was found to exhibit these properties. Securinine (30 microM) induces apoptosis in 73% of p53-null HCT116 cells (LD(50) 17.5 microM) as opposed to 17.6% of HCT116 parental cells (LD(50) 50 microM) at 72 h after treatment. The mechanism of securinine-mediated death in p53-deficient cells involves the induction of the p53 family member, p73. Interestingly, the proapoptotic protein p73 is down-regulated in colon cancer cells expressing p53. This differential regulation of p73 in a p53-dependent fashion reveals a novel pathway for preferentially targeting cancer cells. In contrast to p53-deficient cells, cells expressing p53 are protected from cell death through the p53-mediated up-regulation of p21. These studies reveal a novel approach to specifically target colon cancer cells lacking p53 as well as identify a novel clinically relevant pathway to selectively induce p73 in p53-null cells.
Authors:
Sonia Rana; Kalpana Gupta; Jose Gomez; Shigemi Matsuyama; Amitabha Chakrabarti; Munna L Agarwal; Anju Agarwal; Mukesh K Agarwal; David N Wald
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Publication Detail:
Type:  Journal Article     Date:  2010-02-04
Journal Detail:
Title:  FASEB journal : official publication of the Federation of American Societies for Experimental Biology     Volume:  24     ISSN:  1530-6860     ISO Abbreviation:  FASEB J.     Publication Date:  2010 Jun 
Date Detail:
Created Date:  2010-06-02     Completed Date:  2010-07-21     Revised Date:  2012-02-15    
Medline Journal Info:
Nlm Unique ID:  8804484     Medline TA:  FASEB J     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2126-34     Citation Subset:  IM    
Affiliation:
Invenio Therapeutics, Cleveland, Ohio, USA.
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MeSH Terms
Descriptor/Qualifier:
Apoptosis / drug effects*
Azepines / pharmacology*
Blotting, Western
Caspases / antagonists & inhibitors,  metabolism
Cell Adhesion / drug effects
Cell Cycle / drug effects
Cell Proliferation / drug effects
Colonic Neoplasms / drug therapy,  metabolism*,  pathology*
DNA Damage / drug effects
DNA-Binding Proteins / genetics,  metabolism*
Heterocyclic Compounds with 4 or More Rings / pharmacology
Humans
Lactones / pharmacology*
Nuclear Proteins / genetics,  metabolism*
Piperidines / pharmacology*
RNA, Messenger / genetics,  metabolism
Reverse Transcriptase Polymerase Chain Reaction
Tumor Cells, Cultured
Tumor Suppressor Protein p53 / genetics,  metabolism*
Tumor Suppressor Proteins / genetics,  metabolism*
Chemical
Reg. No./Substance:
0/Azepines; 0/DNA-Binding Proteins; 0/Heterocyclic Compounds with 4 or More Rings; 0/Lactones; 0/Nuclear Proteins; 0/Piperidines; 0/RNA, Messenger; 0/TP53 protein, human; 0/Tumor Suppressor Protein p53; 0/Tumor Suppressor Proteins; 0/tumor suppressor protein p73; 5610-40-2/securinine; EC 3.4.22.-/Caspases

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


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