MicroRNAs 221 and 222 inhibit normal erythropoiesis and erythroleukemic cell growth via kit receptor down-modulation.
By N. Felli, L. Fontana, E. Pelosi, R. Botta, D. Bonci, F. Facchiano, F. Liuzzi, V. Lulli, O. Morsilli, Simona Santoro and 6 more. Proceedings of the National Academy of Sciences of the United States of America, 2005
795 citations recorded by the source corpus.
Subfields: Cancer Research, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/5631e50fd39d9c7a54dec2bb5e5a016f8402c8b5
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In Cancer Research
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Citations in the corpus
- Physiological and pathological roles for microRNAs in the immune system (2010, background): “miR-221 and miR-222 were also shown to inhibit KIT expression by stem and progenitor cells, leading to impaired cell proliferation and engraftment potentia”
- MicroRNAs: new regulators of immune cell development and function (2008, background): “In addition, miR-221 and miR-222 are downregulated during erythropoiesis, thus relieving repression of their target, which encodes the stem cell factor receptor c-Ki”
- MicroRNAs: key regulators of stem cells (2009, background): “Another mechanism that prevents erythropoiesis involves miR-221 and miR-222, which block erythropoiesis by targeting KIT (also known as CD117 ), a cytokine receptor that is expressed on the surface of haematopoietic stem cell”
- Identification of miRNA Changes in Alzheimer's Disease Brain and CSF Yields Putative Biomarkers and Insights into Disease Pathways (2008, positive): “Interestingly, miR-221 can inhibit c-Kit expression while miR-10a inhibits the Homeobox gene Hox-A1 and both c-Kit and Hox-A1 have roles in hematopoiesis and T cell development [20,22,69].”
- MicroRNA expression alterations are linked to tumorigenesis and non-neoplastic processes in pancreatic ductal adenocarcinoma (2007, background): “Similarly, it should be possible to correct miRNAs downregulated in tumors using miRNA expression strategies such as viral delivery systems (Felli et al., 2005).”
- Causes and consequences of microRNA dysregulation in cancer (2009, background): “pl?acc=MI0000299">miR-222 target an oncogene, KIT , and inhibit the growth of erythroblastic leukaemi”
- OncomiRs: the discovery and progress of microRNAs in cancers (2007, background): “The decline of miR-221 and miR-222 during exponential erythropoietic growth unblocked Kit protein production at mRNA level, thus leading to expansion of early erythroblasts [26].”
- MicroRNA-133 controls cardiac hypertrophy (2007, background): “MiRNAs are involved in a variety of basic biological processes, for example, cell proliferation and apoptosi”
- MiR-221 controls CDKN1C/p57 and CDKN1B/p27 expression in human hepatocellular carcinoma (2008, background): “Third, miR-221 is selectively upregulated in several human cancers and evidences supporting its role in carcinogenesis and increased cell growth have been reported (Felli et al., 2005; Galardi et al., 2007; Gillies and Lorimer, 2007; Le Sage et al., 2007; Visone et al., 2007).”
- MicroRNAs: key players in the immune system, differentiation, tumorigenesis and cell death (2008, background): “One such observation implicates miR-221 and miR-222 in maintaining hematopoietic stem cells by preventing the formation of early erythroblasts by directly targeting the receptor c-kit (Felli et al., 2005).”