Targeted abrogation of diverse signal transduction cascades by emodin for the treatment of inflammatory disorders and cancer
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Emodin (1,3,8-trihydroxy-6-methylanthraquinone) is a natural occurring anthraquinone derivative isolatedfrom roots and barks of numerous plants, molds, and lichens. It is found as an active ingredientin 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. Theanti-inflammatory effects of emodin have been exhibited in various in vitro as well as in vivo modelsof inflammation including pancreatitis, arthritis, asthma, atherosclerosis and glomerulonephritis. As ananti-cancer agent, emodin has been shown to suppress the growth of various tumor cell lines includinghepatocellular carcinoma, pancreatic, breast, colorectal, leukemia, and lung cancers. Emodin is a pleiotropicmolecule capable of interacting with several major molecular targets including NF-jB, casein kinaseII, HER2/neu, HIF-1a, AKT/mTOR, STAT3, CXCR4, topoisomerase II, p53, p21, and androgen receptorswhich are involved in inflammation and cancer. This review summarizes reported anti-inflammatoryand anti-cancer effects of emodin, and re-emphasizes its potential therapeutic role in the treatment ofinflammatory diseases and cancer.
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An anthraquinone derivative, emodin sensitizes hepatocellular carcinoma cells to TRAIL induced apoptosis through the induction of death receptors and downregulation of cell survival proteinsSubramaniam, Aruljothi; Loo, Ser; Rajendran, P.; Manu, K.; Permul, E.; Li, F.; Shanmugam, M.; Siveen, K.; Park, J.; Ahn, K.; Hui, K.; Kumar, Alan Prem; Sethi, G. (2013)Recombinant tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is currently under clinical trials for cancer, however many tumor cells, including hepatocellular carcinoma (HCC) develop resistance to TRAIL-induced ...
Emodin inhibits growth and induces apoptosis in an orthotopic hepatocellular carcinoma model by blocking activation of STAT3Subramaniam, A.; Shanmugam, M.; Ong, T.; Li, F.; Perumal, E.; Chen, L.; Vali, S.; Abbasi, T.; Kapoor, S.; Ahn, K.; Kumar, Alan Prem; Hui, K.; Sethi, G. (2013)BACKGROUND AND PURPOSE: Aberrant activation of STAT3 is frequently encountered and promotes proliferation, survival, metastasis and angiogenesis in hepatocellular carcinoma (HCC). Here, we have investigated whether emodin ...
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