Expression and function of members of the cytokine receptor superfamily on breast cancer cells

Douglas, Andrea M.; Goss, Geraldine A.; Sutherland, R. L.; Hilton, Douglas J.; Berndt, Michael C.; Nicola, Nicos A.; Begley, C. Glenn

doi:10.1038/sj.onc.1200882

Cited by 91 publications

(63 citation statements)

References 24 publications

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“…Furthermore, both cytokines mediate growth stimulation of myeloma and plasmacytoma cells, but growth inhibition and di erentiation of mouse M1 myeloid leukemia cells. Also certain breast and lung cancer cells respond with growth arrest to IL-6 and OSM (Chen et al, 1988;Douglas et al, 1997;Horn et al, 1990;Takizawa et al, 1993). Besides that, an anti-proliferative e ect of IL-6 and OSM has been described for melanocytes (Swope et al, 1991) and for melanoma cells from early phases of tumor growth (Lu et al, 1992(Lu et al, , 1993(Lu et al, , 1996Swope et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

Interleukin-6 and oncostatin M-induced growth inhibition of human A375 melanoma cells is STAT-dependent and involves upregulation of the cyclin-dependent kinase inhibitor p27/Kip1

Heinrich²,

et al. 1999

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Interleukin-6 (IL-6)-type cytokines lead to growth arrest of human A375 melanoma cells. The present study demonstrates that this e ect depends on the activation of STAT transcription factors. We observed a correlation between the extent of growth inhibition exerted by IL-6, IL-6 plus soluble IL-6 receptor or oncostatin M (OSM) and the intensities of STAT3 and STAT1 signals. A truncated chimeric receptor retaining only the membrane-proximal region of gp130, the common signal transducer of IL-6-type cytokines, did neither activate STATs nor mediate growth arrest of stable transfectants. These functions were restored by the addition of short STAT recruitment modules comprising critical tyrosine residues from gp130 (Y767, Y814). A receptor carrying tyrosine module Y759 of gp130 e ectively mediated activation of the phosphatase SHP-2 but did not alter cell growth. Overexpression of dominant negative forms of STAT3 but not STAT1 abrogated the inhibitory e ect of OSM and IL-6 in A375 cells. In addition, we have identi®ed the cyclin-dependent kinase inhibitor p27/Kip1 as a novel target to be regulated by IL-6-type cytokines. Stimulation-dependent upregulation of p27 mRNA occurred STAT3-dependently. Also p27 protein accumulated which coincided with the disappearance of hyperphosphorylated retinoblastoma protein in three human melanoma cell lines sensitive to IL-6-type cytokines.

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Section: Introductionmentioning

confidence: 99%

Interleukin-6 and oncostatin M-induced growth inhibition of human A375 melanoma cells is STAT-dependent and involves upregulation of the cyclin-dependent kinase inhibitor p27/Kip1

Heinrich²,

et al. 1999

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“…It has been shown that LIF is expressed and secreted from cells with human melanomas (Paglia et al, 1995). Recent research reports possible involvement of the LIF and LIFreceptor in regulating the growth of breast cancer cells (Douglas et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Molecular cloning and functional analysis of cDNA encoding a rat leukemia inhibitory factor: towards generation of pluripotent rat embryonic stem cells

Takahama¹,

Ochiya²,

Sasaki³

et al. 1998

Oncogene

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Embryonic stem (ES) cells are pluripotent cell lines established directly from the early embryo. Maintenance of the stem-cell phenotype of ES cells in vitro requires the presence of a feeder layer of ®broblasts or of a soluble factor, di erentiation inhibitory activity (DIA) such as leukemia inhibitory factor (LIF). Here we report the cloning of complete rat LIF cDNA and its nucleotide sequence so as to facilitate studies of rat ES cell technologies on tumor biology. The nucleotide sequence of the rat LIF cDNA indicated that the rat LIF has 91% amino acid sequence identity with murine LIF. The cloned rat LIF cDNA has a putative biological activity as a di erentiation-inducing factor on the murine myeloid leukemia cell line M1 cells. Culture supernatant of the rat LIF cDNA-transduced rat ®broblast cell line could maintain the stem-cell phenotype of rat ES cells which showed alkaline phosphatase activity, and this e ect was much stronger than that by murine LIF. The availability of rat LIF which shows DIA will assist the in vitro analysis of rat ES cells, and culture of these cells is a route for the generation of gene targeting in rat.

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“…OSM belongs to the interleukin-6 family, which includes interleukin-6, interleukin-11, ciliary neurotrophic factor, cardiotrophin-1, and leukemia inhibitory factor (3)(4)(5)(6). Recently, OSM has been demonstrated to have a bifunctional activity: an antiproliferative effect on a variety of solid tumor cell lines, such as breast cancer (7,8), melanoma (9), meningioma (10), and lung carcinoma (11), and a proliferative effect on cells from acquired immunodeficiency syndrome (AIDS)-related Kaposi's sarcoma (12,13) and multiple myeloma (14,15). The biologic effects of OSM in the pathogenesis of cutaneous epithelial tumors have not been explored.…”

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confidence: 99%

Comparison of Oncostatin M Expression in Keratoacanthoma and Squamous Cell Carcinoma

et al. 2000

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Oncostatin M (OSM) is a 28-kDa glycoprotein, produced by stimulated macrophages and T lymphocytes, that inhibits the proliferation and induces differentiation of a number of different cell lines derived from solid tumors. To determine whether keratoacanthoma (KA) is unique or a variant of squamous cell carcinoma (SCC), we compared the immunohistochemical expression of OSM in the tumor cells and peri-and intratumoral macrophages of 21 mature KAs, 7 regressing KAs, and 27 SCCs. An inverse correlation was identified between OSM tumor labeling and the density of OSM-labeled tumor-associated macrophages for KAs (r ‫؍‬ ؊.4; P ‫؍‬ .09). OSM tumor expression was significantly more frequent and more intense in KAs than in SCCs (95% versus 63%; P < .01). In contrast, the density of OSM-labeled macrophages was significantly higher in SCCs compared with mature KAs (7/3 high power fields versus 4/3 high power fields; P ‫؍‬ .02). These OSM-positive macrophages were predominantly located at the advancing, infiltrative margins of both neoplasms. Regressing KAs demonstrated a decreased level of OSM tumor expression compared with mature KAs (53% versus 95%; P ‫؍‬ .001), but there was no difference in density of OSMlabeled macrophages. Both the above differences and the overlapping patterns of OSM expression suggest that KAs are a variant of SCC where OSM, possibly as an autocrine factor, may mediate KA's overwhelming but not absolute tendency to involute.

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Expression and function of members of the cytokine receptor superfamily on breast cancer cells

Cited by 91 publications

References 24 publications

Interleukin-6 and oncostatin M-induced growth inhibition of human A375 melanoma cells is STAT-dependent and involves upregulation of the cyclin-dependent kinase inhibitor p27/Kip1

Interleukin-6 and oncostatin M-induced growth inhibition of human A375 melanoma cells is STAT-dependent and involves upregulation of the cyclin-dependent kinase inhibitor p27/Kip1

Molecular cloning and functional analysis of cDNA encoding a rat leukemia inhibitory factor: towards generation of pluripotent rat embryonic stem cells

Comparison of Oncostatin M Expression in Keratoacanthoma and Squamous Cell Carcinoma

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