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Inhibitory effect of baicalein on IL‐6‐mediated signaling cascades in human myeloma cells
Author(s) -
Liu Shangqin,
Ma Zi,
Cai Huili,
Li Qian,
Rong Wenyu,
Kawano Michio
Publication year - 2010
Publication title -
european journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0902-4441
DOI - 10.1111/j.1600-0609.2009.01365.x
Subject(s) - baicalein , multiple myeloma , signal transduction , cancer research , inhibitory postsynaptic potential , microbiology and biotechnology , neuroscience , chemistry , immunology , medicine , pharmacology , biology
Interleukin‐6 (IL‐6) is an important growth factor for myeloma cells. IL‐6 promotes the survival and proliferation of multiple myeloma (MM) cells through the phosphorylated proteins, including STAT3, MAPK, and Akt. Chemical components that suppress the signaling proteins’ phosphorylation have a potential role for MM therapy. We recently identified that baicalein, a component of Scutellaria radix , suppressed proliferation and induced apoptosis of myeloma cells by blocking IκB‐α degradation followed by down‐regulating IL‐6 and XIAP gene expression. In the present study of four myeloma cell lines, namely U266, NOP2, AMO1, and ILKM2, we demonstrated that baicalein not only inhibited IL‐6‐mediated phosphorylation of signaling proteins, such as Jak, STAT3, MAPK, and Akt, but also inhibited the expression of their target genes, such as bcl‐xl . Finally, baicalein facilitated myeloma cell proliferation inhibited by dexamethasone. In contrast, baicalin, another major flavonoid derived from Scutellaria radix , had no significant effect on IL‐6‐mediated protein phosphorylation. Baicalein had no effect on Akt phosphorylation induced by the insulin‐like growth factor‐1 (IGF‐1) in NOP2 cells. Compared with PD98059, an MAPK inhibitor, baicalein exhibited a stronger inhibitory effect on Erk 1/2 phosphorylation. Our results demonstrate that baicalein is a potent inhibitor of protein phosphorylation induced by IL‐6, and thus may be a useful agent for the treatment of MM.