Oroxylin A Prevents Inflammation-Related Tumor Through Down-Regulation of Inflammatory Gene Expression by Inhibiting NF-κB Signaling

被引:51
|
作者
Yao, Jing [1 ]
Hu, Rong [2 ]
Sun, Jie [1 ]
Lin, Biqi [2 ]
Zhao, Li [1 ]
Sha, Yunying [1 ]
Zhu, Binbin [1 ]
You, Qi-Dong [2 ]
Yan, Tianhua [3 ]
Guo, Qing-Long [1 ]
机构
[1] China Pharmaceut Univ, State Key Lab Nat Med, Jiangsu Key Lab Carcinogenesis & Intervent, Nanjing 210009, Jiangsu, Peoples R China
[2] China Pharmaceut Univ, Sch Pharm, Nanjing 210009, Jiangsu, Peoples R China
[3] China Pharmaceut Univ, Dept Physiol, Nanjing 210009, Jiangsu, Peoples R China
关键词
oroxylin A; inflammatory cytokines; NF-kappa B; chemoprevention; IN-VITRO; CANCER DEVELOPMENT; ANTITUMOR-ACTIVITY; SCUTELLARIA-RADIX; INDUCED APOPTOSIS; NITRIC-OXIDE; WOGONIN; MICROENVIRONMENT; CELLS; BAICALEIN;
D O I
10.1002/mc.21958
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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-B p65 nuclear translocation and phosphorylation of IB and IKK/ 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-1, 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-B signaling pathway involved in inflammation-induced cancer initiation and progression and therefore could be a potential cancer chemoprevention agent for inflammation-related cancer. (c) 2012 Wiley Periodicals, Inc.
引用
收藏
页码:145 / 158
页数:14
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