Expression of the c-fms proto-oncogene during human monocytic differentiation

Sariban, Eric; Mitchell, Thomas W.; Küfe, Donald

doi:10.1038/316064a0

Cited by 262 publications

(125 citation statements)

References 31 publications

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“…TPA induces both HL-60 and U-937 cells to differentiate along the monocytic lineage [6,7]. This differentiation is associated with a decrease in c-myc expression [6,7].…”

Section: Introductionmentioning

confidence: 99%

Inhibition of protein kinase C is associated with a decrease in c‐myc expression in human myeloid leukemia cells

et al. 1991

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Treatment of human myeloid leukemic cells with phorbol esters such as 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA) is associated with activation and then partial down‐regulation of protein kinase C activity. Previous work has suggested that the activation of protein kinase C by TPA contributes to the decrease in c‐myc expression during differentiation of these cells. The present studies demonstrate that the decline in c‐myc mRNA levels following exposure of HL‐60 cells to TPA is preceded by an increase in expression of this gene. In contrast, exposure of HL‐60 cells to inhibitors of protein kinase C activity is associated with down‐modulation of c‐myc expression. Similar findings have been obtained in U‐937 myeloid leukemia cells. Taken together, these findings suggest that phorbol esters have a biphasic effect on c‐myc expression. Whereas the activation of protein kinase C by phorbol esters may be associated with an increase in c‐myc gene expression, the subsequent partial down‐regulation of kinase activity may initiate a cascade of events resulting in the down‐modulation of c‐myc expression.

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“…TPA induces both HL-60 and U-937 cells to differentiate along the monocytic lineage [6,7]. This differentiation is associated with a decrease in c-myc expression [6,7].…”

Section: Introductionmentioning

confidence: 99%

Inhibition of protein kinase C is associated with a decrease in c‐myc expression in human myeloid leukemia cells

et al. 1991

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“…In addition, nonc of the induced highly malignant neoplasms contained detectable amounts of Xfm.rt transcripts. In mammals, CSF-1 R is onc of the factors playing an important rolc during maturation and growth activation of macrophages (Sariban et al, 1985;Sherr, 1988;Sherr et a/., 1985). Macraphages are present at places that give rise to infection.…”

Section: Expression In Chemica/ly Induced Neoplasms Of Xiphophorusmentioning

confidence: 99%

Different expression patterns of oncogenes and proto‐oncogenes in hereditary and carcinogen‐induced tumors of xiphophorus

Mäueler

Schartl

1993

Intl Journal of Cancer

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Hereditary melanoma in Xiphophorus hybrids carrying the melanoma‐inducing Tu‐Sd locus is caused by transcriptional activation of the Xmrk gene that resides at the Tu‐Sd locus and encodes a novel member of receptor tyrosine kinases (RTK). In this study, a total of 27 hereditary melanomas from various hybrid genotypes harbouring 7 different Tu alleles were also found to over‐express the corresponding Xmrk alleles. The level of over‐expression correlated with the degree of malignancy of the melanoma. In addition, Xsrc expression was high in many malignant melanomas. Expression patterns and levels of the Xiphophorus EGF‐receptor gene (Xerb B), the c‐myc (Xmyc), and the PDGF (Xsis) gene(s) were not intriguing. Transcription of the ras gene(s) may be correlated to secondary events of melanoma progression. Expression patterns of Xfms, the Xiphophorus CSF‐I receptor homologue, can be explained by different contents of infiltrating macrophages in the tumors. In carcinogen‐induced tumors including one melanoma no significant expression of the Xmrk oncogene could be detected. Xsrc expression, however, was strikingly high. This indicates that activation of oncogenes other than Xmrk is instrumental in tumorigenesis of neoplasia of non‐hereditary origin.

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“…The gene is the cellular counterpart of the feline sarcoma virus v-fms (Sherr et al, 1985). It was first linked to monocytic differentiation when transcripts were identified in peripheral blood monocytes, and monocytic, but not granulocytic, differentiation of HL60 cells was accompanied by upregulation of c-FMS expression (Sariban et al, 1985). Low levels of mRNA transcripts can be detected in haematopoietic progenitor cells, although cell surface expression of the protein does not become detectable until later in monocytic differentiation (Tagoh et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

c-FMS chromatin structure and expression in normal and leukaemic myelopoiesis

et al. 2005

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The macrophage colony-stimulating factor receptor is encoded by the c-FMS gene, and it has been suggested that altered regulation of c-FMS expression may contribute to leukaemic transformation. c-FMS is expressed in pluripotent haemopoietic precursor cells and is subsequently upregulated during monocytic differentiation, but downregulated during granulopoiesis. We have examined transcription factor occupancy and aspects of chromatin structure of the critical c-FMS regulatory element located within the second intron (FIRE -fms intonic regulatory element) during normal and leukaemic myelopoiesis. Granulocytic differentiation from normal and leukaemic precursors is accompanied by loss of transcription factors at FIRE and downregulated c-FMS expression. The presence of AML1-ETO in leukaemic cells does not prevent this disassembly. In nonleukaemic cells, granulocytic differentiation is accompanied by reversal to a chromatin fine structure characteristic of c-FMS-nonexpressing cells. In addition, we show that lowlevel expression of the gene in leukaemic blast cells and granulocytes does not associate with increased CpG methylation across the c-FMS locus.

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Expression of the c-fms proto-oncogene during human monocytic differentiation

Cited by 262 publications

References 31 publications

Inhibition of protein kinase C is associated with a decrease in c‐myc expression in human myeloid leukemia cells

Inhibition of protein kinase C is associated with a decrease in c‐myc expression in human myeloid leukemia cells

Different expression patterns of oncogenes and proto‐oncogenes in hereditary and carcinogen‐induced tumors of xiphophorus

c-FMS chromatin structure and expression in normal and leukaemic myelopoiesis

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