Journal
JOURNAL OF NUTRITIONAL BIOCHEMISTRY
Volume 23, Issue 7, Pages 706-715Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jnutbio.2011.03.013
Keywords
4-O-methylhonokiol; NF-kappa B; p21; Cancer cells; Growth inhibition
Funding
- Korea Research Foundation Grant (MRC) [R13-2008-001-00000-00]
- Korea Ministry of Education, Science and Technology (The Regional Core Research Program/Chunbuk BIT Research-Oriented University Consortium)
- National Research Foundation of Korea [2008-0062259] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Biphenolic components in the Magnolia family have shown several pharmacological activities such as antitumor effects. This study investigated the effects of 4-O-methylhonokiol (MH), a constituent of Magnolia officinalis, on human colon cancer cell growth and its action mechanism. 4-O-methylhonokiol (0-30 mu M) decreased constitutive activated nuclear factor (NF)-kappa B DNA binding activity and inhibited growth of human colon (SW620 and HCT116) cancer cells. It also caused G(0)-G(1) phase cell cycle arrest followed by an induction of apoptotic cell death. However, knockdown with small interfering RNA (siRNA) of p21 or transfection with cyclin D1/Cdk4 binding site-mutated p21 abrogated MH-induced cell growth inhibition, inhibition of NF-kappa B activity as well as expression of cyclin D1 and Cdk4. Conversely, inhibition of NF-kappa B with specific inhibitor or siRNA augmented MH-induced apoptotic cell death. 4-O-methylhonokiol inhibited tumor growth, NF-kappa B activity and expression of antiapoptotic proteins; however, it increased the expression of apoptotic proteins as well as p21 in xenograft nude mice bearing SW620 cancer cells. The present study reveals that MH causes p21-mediated human colon cancer cell growth inhibition through suppression of NF-kappa B and indicates that this compound by itself or in combination with other anticancer agents could be useful for the treatment of cancer. (C) 2012 Elsevier Inc. All rights reserved.
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