Selective expression of FLIP in malignant melanocytic skin lesions
Details
Serval ID
serval:BIB_DEC537B94C9E
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Selective expression of FLIP in malignant melanocytic skin lesions
Journal
Journal of Investigative Dermatology
ISSN
0022-202X (Print)
Publication state
Published
Issued date
08/2001
Volume
117
Number
2
Pages
360-4
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Aug
Research Support, Non-U.S. Gov't --- Old month value: Aug
Abstract
FLIP (FLICE Inhibitory Protein) is a recently identified intracellular inhibitor of caspase-8 activation that potently inhibits cell death mediated by all death receptors including Fas and TRAIL. FLIP has recently been shown to favor tumor growth and immune escape in mouse tumor models. We analyzed FLIP expression by immunohistochemistry in a panel of 61 benign and malignant human melanocytic skin lesions. FLIP expression was undetectable in all but one benign melanocytic lesion (31/32, 97%). In contrast, FLIP was strongly expressed in most melanomas (24/29 = 83%). Overexpression of FLIP by transfection in a Fas- and TRAIL-sensitive human melanoma cell line rendered this cell line more resistant to death mediated by both TRAIL and FasL. Selective expression of FLIP by human melanomas may confer in vivo resistance to FasL and TRAIL, thus representing an additional mechanism by which melanoma cells escape immune destruction.
Keywords
Antibody Specificity
*Apoptosis
Apoptosis Regulatory Proteins
CASP8 and FADD-Like Apoptosis Regulating Protein
Carrier Proteins/analysis/*genetics/immunology
Fas Ligand Protein
*Gene Expression Regulation, Neoplastic
Humans
Immunohistochemistry
*Intracellular Signaling Peptides and Proteins
Melanoma/*physiopathology
Membrane Glycoproteins/analysis/genetics
Nevus
Skin Neoplasms/*physiopathology
TNF-Related Apoptosis-Inducing Ligand
Transfection
Tumor Cells, Cultured
Tumor Necrosis Factor-alpha/analysis/genetics
Pubmed
Web of science
Open Access
Yes
Create date
24/01/2008 16:19
Last modification date
20/08/2019 17:03