SMAD proteins control DROSHA-mediated microRNA maturation

By Brandi N. Davis, A. Hilyard, G. Lagna, A. Hata. Nature, 2008

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MicroRNAs: New Biomarkers for Diagnosis, Prognosis, Therapy Prediction and Therapeutic Tools for Breast Cancer (2015, background): “Thus, tumorigenic miRNA expression alterations could be due to the activity of tumor-related transcription factors, such as SMAD [90, 95], p53 protein family (p53, p63, and p73) [96], ataxia telangiectasia mutated (ATM) [97], and Myc [98].”
Posttranscriptional regulation of microRNA biogenesis in animals. (2010, background): “Treatment of human vascular smooth muscle cells with either bone morphogenetic protein 4 (BMP4) or transforming growth factor beta (TGF-b) stimulates SMAD binding to p68 and increases Drosha processing of pri-miR-21 and pri-miR-199a (Davis et al., 2008).”
EMT, cancer stem cells and drug resistance: an emerging axis of evil in the war on cancer (2010, background): “Initially, Smad proteins can directly regulate microRNA processing by binding to the DROSHA complex, which has been shown for mir-21 (Davis et al., 2008).”
TGFβ in Cancer (2008, background): “In a remarkable new finding, BMP-activated Smad1 and TGFβ-activated Smad2/3 bind to p68, a component of the microRNA (miRNA) processing complex DROSHA, to target the primary miR-21 transcript (primiR-21) for miR-21 production in vascular smooth muscle cells (Davis et al., 2008).”