Abstract
We studied the production of macrophage colony-stimulating factor (M-CSF) and the expression of c-fms mRNA, an M-CSF receptor, in four human ovarian cancer cell lines. All four cell lines expressed c-fms mRNA while three secreted M-CSF into the culture medium. The exogenous administration of M-CSF caused no significant enhancement of cellular proliferation in any cell line. Interestingly, the proliferation of KK cells was not affected by anti-M-CSF antibody. These results, taken together with the fact that ovarian cancer cells simultaneously produce M-CSF and c-fms, suggest that an autocrine mechanism may modulate cellular proliferation.
MeSH terms
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Adenocarcinoma / metabolism*
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Adenocarcinoma / pathology
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Antibodies, Anti-Idiotypic / pharmacology
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Cell Division / drug effects
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Female
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Humans
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Macrophage Colony-Stimulating Factor / biosynthesis*
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Macrophage Colony-Stimulating Factor / immunology
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Macrophage Colony-Stimulating Factor / pharmacology
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Oncogene Protein gp140(v-fms) / biosynthesis*
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Ovarian Neoplasms / metabolism*
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Ovarian Neoplasms / pathology
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Proto-Oncogene Mas
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RNA, Messenger / biosynthesis*
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Tumor Cells, Cultured
Substances
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Antibodies, Anti-Idiotypic
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MAS1 protein, human
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Oncogene Protein gp140(v-fms)
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Proto-Oncogene Mas
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RNA, Messenger
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Macrophage Colony-Stimulating Factor