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Regulus Therapeutics to Present New Advancements in microRNA Therapeutics for Treatment of Metabolic Diseases and Cancer
Date:9/8/2011

ch differ by only two nucleotides, are intronic microRNAs located within the sterol response element binding protein genes SREBF2 and SREBF1, respectively, which code for transcription factors that regulate cholesterol and fatty acid metabolism. Recent studies have shown that miR-33a/b regulates the cholesterol and fatty acid pathways in a negative feedback loop.  miR-33/b represses the cholesterol transporter ABCA1 resulting in decreased cellular cholesterol efflux to HDL-C and reverse cholesterol transport. Inhibition of miR-33 in mice, which only have miR-33a, resulted in enhanced cholesterol transport and reduction of atherosclerotic plaques (Rayner et al., J Clin Invest doi:10.1172/JCI57275). miR-33a/b also suppresses key enzymes involved in the oxidation of fatty acids resulting in the accumulation of triglycerides. Inhibition of miR-33a/b increases fatty acid oxidation and insulin signaling (Davalos et al., PNAS doi:10.1073/pnas.1102281108). These studies suggest that an anti-miR33a/b oligonucleotide treatment may be a promising strategy to treat metabolic disease.  

miR-21.  Regulus is developing microRNA therapeutics targeting miR-21 using proprietary chemically modified anti-miR oligonucleotides delivered systemically. Recent studies have demonstrated that miR-21 is overexpressed in many cancer types (Volinia et al., PNAS. 2006) and can promote tumor progression and metastasis (Medina et al., Nature. 2010). Regulus data has shown that miR-21 is upregulated in patients with hepatocellular carcinoma (HCC). In preclinical models of HCC, short term treatment (2-3 weeks) with anti-miR-21 inhibited miR-21 in the liver and reduced liver tumor formation. Longer term treatment (17 weeks) with anti-miR-21 resulted in a significant survival advantage (p<0.0001) over saline and control anti-miR treated mice. These findings suggest that miR-21 is a promising target for cancer.


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