Stephania delavayi Diels. inhibits breast carcinoma proliferation through the p38 MAPK/NF-kappa B/COX-2 pathway

作者:Park Dae Hun; De Xu Hong; Shim Jaegal; Li Yong Chun; Lee Jong Hwa; Cho Soon Chang; Han Sang Seop; Lee Yun Lyul; Lee Min Jae*; Kwon Sung Won
来源:Oncology Reports, 2011, 26(4): 833-841.
DOI:10.3892/or.2011.1364

摘要

The nuclear factor kappa B (NF-kappa B)/inhibitor of K kinase-beta (IKK beta) signaling pathway is important in tumor promotion and progression. MDA-MB-231 human breast carcinoma cells express COX-2 and show a constitutive phosphorylation of NF-kappa B. Many non-specific inhibitors of IKK beta and NF-kappa B are used to inhibit tumor promotion and progression. The Stephania delavayi Die Is. (S. delavayi Die Is.) extract has been reported to safely activate B cell immunity and there is evidence suggesting that it may be a promising new anticancer therapeutic agent. S. delavayi Die Is. extract suppressed proliferation of the breast cancer cell lines MDA-MB-231 and MCF-7 by inducing cell death. To aid in the development of the S. delavayi Diels. extract as a therapeutic agent, its mechanisms of action were investigated, in particular its effects on p38 MAPK, NF-kappa B and COX-2, which play important roles in inflammation and cancer. S. delavayi Die Is. stimulated p38 MAPK phosphorylation but reduced NF-kappa B phosphorylation and COX-2 expression in a dose- and time-dependent manner. Thus, S. delavayi Die Is., which appears to act primarily through p38 MAPK/NF-kappa B/COX-2 signaling in breast carcinomas, may be a potent anticancer agent with target specificity and low toxicity.