Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.canlet.2013.08.023
Title: Targeted abrogation of diverse signal transduction cascades by emodin for the treatment of inflammatory disorders and cancer
Authors: Shrimali, D.
Shanmugam, M.K. 
Kumar, A.P. 
Zhang, J.
Tan, B.K.H.
Ahn, K.S.
Sethi, G.
Keywords: Angiogenesis
Apoptosis
Cancer
Emodin
Metastasis
Issue Date: 1-Dec-2013
Citation: Shrimali, D., Shanmugam, M.K., Kumar, A.P., Zhang, J., Tan, B.K.H., Ahn, K.S., Sethi, G. (2013-12-01). Targeted abrogation of diverse signal transduction cascades by emodin for the treatment of inflammatory disorders and cancer. Cancer Letters 341 (2) : 139-149. ScholarBank@NUS Repository. https://doi.org/10.1016/j.canlet.2013.08.023
Abstract: Emodin (1,3,8-trihydroxy-6-methylanthraquinone) is a natural occurring anthraquinone derivative isolated from roots and barks of numerous plants, molds, and lichens. It is found as an active ingredient in different Chinese herbs including Rheum palmatum and Polygonam multiflorum, and has diuretic, vasorelaxant, anti-bacterial, anti-viral, anti-ulcerogenic, anti-inflammatory, and anti-cancer effects. The anti-inflammatory effects of emodin have been exhibited in various in vitro as well as in vivo models of inflammation including pancreatitis, arthritis, asthma, atherosclerosis and glomerulonephritis. As an anti-cancer agent, emodin has been shown to suppress the growth of various tumor cell lines including hepatocellular carcinoma, pancreatic, breast, colorectal, leukemia, and lung cancers. Emodin is a pleiotropic molecule capable of interacting with several major molecular targets including NF-κB, casein kinase II, HER2/neu, HIF-1α, AKT/mTOR, STAT3, CXCR4, topoisomerase II, p53, p21, and androgen receptors which are involved in inflammation and cancer. This review summarizes reported anti-inflammatory and anti-cancer effects of emodin, and re-emphasizes its potential therapeutic role in the treatment of inflammatory diseases and cancer. © 2013 Elsevier Ireland Ltd.
Source Title: Cancer Letters
URI: http://scholarbank.nus.edu.sg/handle/10635/109814
ISSN: 03043835
DOI: 10.1016/j.canlet.2013.08.023
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