Mechanisms of myeloma cell proliferation induced by interleukin-6

Specific intracellular signals mediated by IL-6 receptor complexes, such as STAT3 and ERK1/2, are considered to be responsible for inducing a variety of cellular responses. In multiple myeloma, IL-6 only enhances the proliferation of CD45^+ tumor cells that harbor the IL-6-independent activation of src family kinases even though STAT3 and ERK1/2 are activated in response to IL-6 in both CD45^+ and CD45^- cells. Furthermore, the IL-6-induced prollferation of CD45^+ U266 myeloma cells is significantly suppressed by Lyn-specific antisense oligodeoxynucleotides or a selective src kinase inhibitor. These results indicate that the activation of both STAT3 and ERK1/2 is not sufficient for IL-6-induced proliferation of myeloma cell llnes that require src family kinase activation independent of IL-6 stimulation. Thus, the activation of the src family kinases associated with CD45 expression is a prerequisite for the proliferation of myeloma cell lines by IL-6. We propose a mechanism for IL-6 induced cell proliferation that is strictly dependent upon the cellular context in myelomas.

骨髄腫

細胞増殖

インターロイキン6 CD45

src型チロシンキナーゼ

本文データは山口大学医学会の許諾に基づきCiNiiから複製したものである