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Oroxylin a prevents inflammation‐related tumor through down‐regulation of inflammatory gene expression by inhibiting NF‐κB signaling
Author(s) -
Yao Jing,
Hu Rong,
Sun Jie,
Lin Biqi,
Zhao Li,
Sha Yunying,
Zhu Binbin,
You QiDong,
Yan Tianhua,
Guo QingLong
Publication year - 2014
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/mc.21958
Subject(s) - inflammation , biology , nf κb , proinflammatory cytokine , iκb kinase , cancer research , signal transduction , tumor microenvironment , lipopolysaccharide , cancer cell , phosphorylation , microbiology and biotechnology , cancer , immunology , tumor cells , genetics
Increasing evidence suggests that inflammatory microenvironment plays a critical role at different stages of tumor development. However, the molecular mechanisms of the interaction between inflammation and proliferation of cancer cells remain poorly defined. Here we reported the inhibitory effects of oroxylin A on the inflammation‐stimulated proliferation of tumor cells and delineated the mechanism of its action. The results indicated that treatment with oroxylin A inhibited NF‐κB p65 nuclear translocation and phosphorylation of IκBα and IKKα/β in both human colon tumor HCT116 cells and human monocytes THP‐1 cells. In addition, in THP‐1 cells, oroxylin A significantly suppressed lipopolysaccharide (LPS)‐induced secretion of prototypical proinflammatory cytokine IL‐6 but not IL‐1β, and it was confirmed at the transcription level. Moreover, oroxylin A inhibited the proliferation of HCT116 cells stimulated by LPS‐induced THP‐1 cells in co‐culture microenvironment. In summary, oroxylin A modulated NF‐κB signaling pathway involved in inflammation‐induced cancer initiation and progression and therefore could be a potential cancer chemoprevention agent for inflammation‐related cancer. © 2012 Wiley Periodicals, Inc.