2007
DOI: 10.1038/sj.onc.1210306
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Inhibition of IL-6-dependent growth of myeloma cells by an acidic peptide repressing the gp130-mediated activation of Src family kinases

Abstract: An acidic domain (AD) of gp130 was previously found to interact with the Src family kinase (SFK) Hck. Here, the influence of myristoylated peptides derived from this AD was assessed in the mouse myeloma cell line, 7TD1. The IL-6-dependent growth of 7TD1 cells was reduced by B75%, if 100 lM of myristoylated 18mer peptide (18AD) was included in the growth medium, but was unaffected by a control peptide with scrambled sequence (18sc). A similar differential inhibition by peptides 18AD and 18sc was observed for th… Show more

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Cited by 24 publications
(14 citation statements)
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“…Src, in conjunction with JAK kinases, may therefore be major upstream cellular pathways regulating the expression of the DNMTs and subsequent methylation. Src also has a well-known oncogenic role and is activated by multiple cytokines including IL-6 (Hausherr et al, 2007).…”
Section: Discussionmentioning
confidence: 99%
“…Src, in conjunction with JAK kinases, may therefore be major upstream cellular pathways regulating the expression of the DNMTs and subsequent methylation. Src also has a well-known oncogenic role and is activated by multiple cytokines including IL-6 (Hausherr et al, 2007).…”
Section: Discussionmentioning
confidence: 99%
“…44 Moreover, kinase-inactive mutants of Hck (K269E or K269R), but not Src (K297R), prevent IL-6-mediated activation of ERK1/2 and inhibit MM-cell proliferation. 15,16 Recently, exposure of serum-starved MM cells to VEGF 165 has been shown to induce activation of Src (manifested by Y418 phosphorylation) and ERK1/2, events abrogated by BMS354825. 17 Such findings suggest that the Src 3 ERK1/2 signaling cascade operates to promote survival mediated by certain growth factors (eg, VEGF and PDGF) in human MM cells.…”
Section: Discussionmentioning
confidence: 99%
“…There is a flurry of new compounds that target IL-6 signaling that are ready to enter the clinical trial arena. These include antibodies to IL-6 and IL-6R, 41 small-molecule IL-6R antagonists, 42 gp130-targeting peptides, 43 and small compounds that target signaling events downstream of the fully assembled, functional IL-6R. Additional therapeutic opportunities are provided by compounds that inhibit pathways that can activate IL-6 signaling indirectly, including NF-B, 44 Hsp90, 45 and PI3K/mTOR inhibitors, 46 or that activate pathways that can inhibit IL-6 signaling indirectly, as described for PPAR␥ inhibitors.…”
Section: Discussionmentioning
confidence: 99%