Document Detail


CD40·FasL and CTLA-4·FasL fusion proteins induce apoptosis in malignant cell lines by dual signaling.
MedLine Citation:
PMID:  21088216     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Evolution of apoptosis resistance in both lymphoma and leukemia cells is well documented, and induction of apoptosis in malignant cells is a major goal of cancer therapy. Up-regulation of anti-apoptotic signals is one of the mechanisms whereby resistance to apoptosis emerges. We have previously described the fusion proteins CD40·FasL and CTLA-4·FasL, which are formed from two functional membrane proteins and induce apoptosis of activated T cells. The present study explores the potential use of CD40·FasL and CTLA-4·FasL for the killing of malignant cells of lymphatic origin. Using malignant B and T cell lines that differ in surface expression of costimulatory molecules, we found that CTLA-4·FasL induces effective apoptosis of cells expressing CD95 and activates caspases 3, 8, and 9. Only B7-expressing B cells responded to CTLA-4·FasL with rapid abrogation of cFLIP expression. CD40·FasL effectively killed only the T cells that express high levels of CD40L in addition to CD95. In these cells, CD40·FasL significantly diminished cFLIP expression. Importantly, each of the fusion proteins is more potent than its respective components parts, alone or in combination. Thus, the proteins with their two functional ends deliver a pro-apoptotic signal and, in parallel, inhibit an anti-apoptotic signal, thus optimizing the wanted, death-inducing effect. Therefore, these proteins emerge as promising agents to be used for targeted and specific tumor cell killing.
Authors:
Ariel Orbach; Jacob Rachmilewitz; Noam Shani; Yonatan Isenberg; Miriam Parnas; Jui-Han Huang; Mark L Tykocinski; Michal Dranitzki-Elhalel
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-11-18
Journal Detail:
Title:  The American journal of pathology     Volume:  177     ISSN:  1525-2191     ISO Abbreviation:  Am. J. Pathol.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-12-01     Completed Date:  2011-03-15     Revised Date:  2011-12-21    
Medline Journal Info:
Nlm Unique ID:  0370502     Medline TA:  Am J Pathol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3159-68     Citation Subset:  AIM; IM    
Affiliation:
Nephrology and Hypertension Services, Hadassah-Hebrew University Medical Center, Jerusalem 91120, Israel.
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MeSH Terms
Descriptor/Qualifier:
Antigens, CD / genetics,  pharmacology*
Antigens, CD40 / genetics,  pharmacology*
Apoptosis / drug effects*
CTLA-4 Antigen
Cell Line, Tumor
Cell Proliferation / drug effects
Cells, Cultured
Drug Evaluation, Preclinical
Fas Ligand Protein / genetics,  pharmacology*
Humans
Jurkat Cells
Molecular Targeted Therapy
Neoplasms / drug therapy,  pathology*
Recombinant Fusion Proteins / genetics,  pharmacology*
Signal Transduction / drug effects
Up-Regulation / drug effects
Chemical
Reg. No./Substance:
0/Antigens, CD; 0/Antigens, CD40; 0/CTLA-4 Antigen; 0/CTLA4 protein, human; 0/Fas Ligand Protein; 0/Recombinant Fusion Proteins

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