| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 1930356 | Biochemical and Biophysical Research Communications | 2011 | 5 Pages |
Inflammatory breast cancer is driven by pro-angiogenic and pro-inflammatory cytokines. One of them Interleukin-6 (IL-6) is implicated in cancer cell proliferation and survival, and promotes angiogenesis, inflammation and metastasis. While IL-6 has been shown to be upregulated by several oncogenes, the mechanism behind this phenomenon is not well characterized. Here we demonstrate that the pleotropic Serine/Threonine kinase CK2 is implicated in the regulation of IL-6 expression in a model of inflammatory breast cancer. We used siRNAs targeted toward CK2 and a selective small molecule inhibitor of CK2, CX-4945, to inhibit the expression and thus suppress the secretion of IL-6 in in vitro as well as in vivo models. Moreover, we report that in a clinical trial, CX-4945 was able to dramatically reduce IL-6 levels in plasma of an inflammatory breast cancer patient. Our data shed a new light on the regulation of IL-6 expression and position CX-4945 and potentially other inhibitors of CK2, for the treatment of IL-6-driven cancers and possibly other diseases where IL-6 is instrumental, including rheumatoid arthritis.
► We examine the potential cross-talk between CK2 and IL-6. ► Inhibition of CK2 by siRNA or CX-4945 inhibits expression of IL-6 in models of IBC. ► Treatment of IBC patient in the clinic with CX-4945 reduces her IL-6 plasma levels. ► We demonstrate that CK2 is a potential therapeutic target for IL-6 driven diseases.
