Augmentation of tumor angiogenesis by a Myc-activated microRNA cluster

By M. Dews, Asal Homayouni, Duonan Yu, D. Murphy, C. Sevignani, Erik A. Wentzel, E. Furth, William Lee, G. Enders, Joshua T. Mendell and 1 more. Nature Genetics, 2006

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MicroRNAs: key players in the immune system, differentiation, tumorigenesis and cell death (2008, background): “Furthermore, c-Myc is known to drive the expression of the pro-tumorigenic miR-17-92 cluster of miRNAs (O’Donnell et al., 2005; Dews et al., 2006), and a high level of c-Myc also leads to a decrease of multiple miRNAs known to have anti-tumorigenic properties (Chang et al., 2008).”
MicroRNA dysregulation in cancer: diagnostics, monitoring and therapeutics. A comprehensive review (2012, neutral): “…ligand Ephrin A3 (Pulkkinen et al, 2008). miR-17-92 cluster sustains MYC angiogenic properties by repressing connective tissue growth factor (CTGF) and anti-angiogenic adhesive glycoprotein thrombospondin 1 (TSP1; Dews et al, 2006), also targeted by miR-27b and let-7f (Kuehbacher et al, 2007).”
Reflecting on 25 years with MYC (2008, background): “Downregulation of thrombospondin is vital to angiogenesis and is potentially achieved through MYC induction of the miR17–92 microRNA cluste”
Genetics of adult glioma. (2012, background): “In addition, the expression of some miRNAs are regulated by transcription factors commonly altered in cancer, such as p53 and c-MYC (55,57,58).”
miRiad roles for the miR-17-92 cluster in development and disease. (2008, background): “Both Tsp1 and CTGF are negatively regulated by these miRNAs, which are potently induced by c-Myc in this model.”