Abstract
Abstract Interleukin-8 (IL-8), a member of CXC subfamily of chemokines, plays important roles in inflammation and cancer. The biological action of IL-8 is mediated through binding to its receptors, CXCR1 (IL-8RA) and CXCR2 (IL-8RB), which are members of the seven transmembrane G-protein-coupled receptor family. Overexpression of IL-8 has been detected in many human tumors, including colon cancer, and it is a major component of the inflammatory tumor microenvironment. Functional studies have shown that IL-8 acts as an autocrine/paracrine growth factor, and promotes growth, invasion, metastasis, angiogenesis and chemoresistance in colon cancer, implying that it could serve as a preventive and therapeutic target. In this study, we examined the effect of honokiol, a biologically active biphenolic compound isolated from the oriental medicinal plant Magnolia officinalis/grandiflora, on two colon cancer cells lines, SW620 and HCT116. Both the cell lines are highly tumorigenic and metastatic, and express high levels of IL-8. Our data demonstrated that honokiol inhibited the expression of IL-8 in both colon cancer cell lines in a dose-dependent manner. IL-8 downregulation by honokiol was also correlated with decreased activation of its transcriptional regulator NF-κB. Honokiol treatment enhanced cytoplasmic accumulation of NF-κB with a concomitant decrease in the nuclear fraction and reduced transcriptional activity of NF-κB-responsive promoter. This was associated with decreased phosphorylation of inhibitor of kappa B alpha (IαB-α) leading to its stabilization and enhanced cytoplasmic levels. In addition, honokiol exerted growth inhibitory effects by inducing apoptosis and G1 phase cell cycle arrest. Altogether, these findings suggest that honokiol could serve as a novel preventive and therapeutic agent in colon cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1626. doi:1538-7445.AM2012-1626
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