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FGF signaling inhibits the proliferation of human myeloma cells and reduces c-myc expression

BACKGROUND: Multiple myeloma is a cancer of antibody producing plasma cells whose etiology is unknown. FGF signaling has been implicated in myeloma pathogenesis but its precise role remains unclear. RESULTS: Here, we investigate the biochemical and phenotypic consequences of FGF stimulation in sever...

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Detalles Bibliográficos
Autores principales: Firme, Louise, Bush, Andrew B
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2003
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC317277/
https://www.ncbi.nlm.nih.gov/pubmed/14656381
http://dx.doi.org/10.1186/1471-2121-4-17
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author Firme, Louise
Bush, Andrew B
author_facet Firme, Louise
Bush, Andrew B
author_sort Firme, Louise
collection PubMed
description BACKGROUND: Multiple myeloma is a cancer of antibody producing plasma cells whose etiology is unknown. FGF signaling has been implicated in myeloma pathogenesis but its precise role remains unclear. RESULTS: Here, we investigate the biochemical and phenotypic consequences of FGF stimulation in several different human myeloma cell lines. We find that FGF signaling inhibits cell cycle progression in two lines and surprisingly, reduces the expression of c-myc while turning on c-fos. In several other lines, FGF signaling does not affect proliferation rate, including cells harboring translocated FGF Receptor 3. When cells are presented with a growth arrest signal, FGF addition induces cell death. CONCLUSIONS: By showing that FGF signaling inhibits mitogenesis and induces apoptosis, we demonstrate novel effects of activating this ubiquitous signaling pathway in multiple myeloma.
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spelling pubmed-3172772004-01-23 FGF signaling inhibits the proliferation of human myeloma cells and reduces c-myc expression Firme, Louise Bush, Andrew B BMC Cell Biol Research Article BACKGROUND: Multiple myeloma is a cancer of antibody producing plasma cells whose etiology is unknown. FGF signaling has been implicated in myeloma pathogenesis but its precise role remains unclear. RESULTS: Here, we investigate the biochemical and phenotypic consequences of FGF stimulation in several different human myeloma cell lines. We find that FGF signaling inhibits cell cycle progression in two lines and surprisingly, reduces the expression of c-myc while turning on c-fos. In several other lines, FGF signaling does not affect proliferation rate, including cells harboring translocated FGF Receptor 3. When cells are presented with a growth arrest signal, FGF addition induces cell death. CONCLUSIONS: By showing that FGF signaling inhibits mitogenesis and induces apoptosis, we demonstrate novel effects of activating this ubiquitous signaling pathway in multiple myeloma. BioMed Central 2003-12-04 /pmc/articles/PMC317277/ /pubmed/14656381 http://dx.doi.org/10.1186/1471-2121-4-17 Text en Copyright © 2003 Firme and Bush; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL.
spellingShingle Research Article
Firme, Louise
Bush, Andrew B
FGF signaling inhibits the proliferation of human myeloma cells and reduces c-myc expression
title FGF signaling inhibits the proliferation of human myeloma cells and reduces c-myc expression
title_full FGF signaling inhibits the proliferation of human myeloma cells and reduces c-myc expression
title_fullStr FGF signaling inhibits the proliferation of human myeloma cells and reduces c-myc expression
title_full_unstemmed FGF signaling inhibits the proliferation of human myeloma cells and reduces c-myc expression
title_short FGF signaling inhibits the proliferation of human myeloma cells and reduces c-myc expression
title_sort fgf signaling inhibits the proliferation of human myeloma cells and reduces c-myc expression
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC317277/
https://www.ncbi.nlm.nih.gov/pubmed/14656381
http://dx.doi.org/10.1186/1471-2121-4-17
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