Document Detail

The variation in Fas localization and the changes in Fas expression level upon stimulation with growth factors.
MedLine Citation:
PMID:  17174268     Owner:  NLM     Status:  MEDLINE    
Although Fas (APO-1/CD95) is well known as a death receptor, its stimulation occasionally fails to induce apoptosis in malignant cells. On the contrary, Fas is reported to advance the cell cycle in cancer cells. Therefore, we investigated roles of Fas in cell growth and apoptosis using human lung cancer cell lines. Fas was localized in the cytoplasm in exponentially growing cells, whereas only confluent cells expressed Fas on the cell membrane. A stimulation of confluent cells by either of EGF, IGF-I or VEGF induced once a decrease in Fas expression level and its sequential recovery. Fas expression levels in confluent cells were negatively correlated with cell doubling times (r=0.757, p=0.0088). Fas remained on the cell membrane of IgM-treated cells even after the growth factor stimulation, leading to apoptosis with abnormal mitosis, whereas the same stimulation induced Fas internalization in IgG(1)-treated cells. From these results, we suggest that Fas remaining on the cell membrane amplifies to induce apoptosis. Conversely, Fas internalization may enable cancer cells to escape from apoptosis. Our results suggest that growth factor may contribute to the resistance of cancer cells to Fas-mediated apoptosis in an autocrine or paracrine fashion.
Kazuki Omoteyama; Shoichi Inoue
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Publication Detail:
Type:  Journal Article     Date:  2006-12-08
Journal Detail:
Title:  Biochemical and biophysical research communications     Volume:  353     ISSN:  0006-291X     ISO Abbreviation:  Biochem. Biophys. Res. Commun.     Publication Date:  2007 Feb 
Date Detail:
Created Date:  2006-12-25     Completed Date:  2007-02-06     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0372516     Medline TA:  Biochem Biophys Res Commun     Country:  United States    
Other Details:
Languages:  eng     Pagination:  159-63     Citation Subset:  IM    
Department of Anatomy, Nihon University School of Dentistry, 1-8-13 Kanda-Surugadai, Tokyo 101-8310, Japan.
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MeSH Terms
Antigens, CD95 / metabolism*
Cell Line, Tumor
Cell Proliferation / drug effects
Dose-Response Relationship, Drug
Gene Expression Regulation, Neoplastic / drug effects*
Intercellular Signaling Peptides and Proteins / administration & dosage*
Lung Neoplasms / metabolism*,  pathology
Subcellular Fractions / drug effects,  metabolism*,  ultrastructure
Reg. No./Substance:
0/Antigens, CD95; 0/FAS protein, human; 0/Intercellular Signaling Peptides and Proteins

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