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PLC-beta 1 regulates the expression of miR-210 during mithramycin-mediated erythroid differentiation in K562 cells (Articolo in rivista)

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PLC-beta 1 regulates the expression of miR-210 during mithramycin-mediated erythroid differentiation in K562 cells (Articolo in rivista) (literal)

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Bavelloni A, Poli A, Fiume R, Blalock W, Matteucci A, Ramazzotti G, McCubrey J.A, Cocco L, Faenza I. (2014)
PLC-beta 1 regulates the expression of miR-210 during mithramycin-mediated erythroid differentiation in K562 cells
in Oncotarget
(literal)

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Bavelloni A, Poli A, Fiume R, Blalock W, Matteucci A, Ramazzotti G, McCubrey J.A, Cocco L, Faenza I. (literal)

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SC Laboratory of Musculoskeletal Cell Biology, Rizzoli Orthopedic Institute, Bologna, Italy; Laboratory RAMSES, Rizzoli Orthopedic Institute, Bologna, Italy; Cell Signaling Laboratory, Department of Biomedical Sciences, University of Bologna, Bologna, Italy; CNR-National Research Council of Italy, Institute of Molecular Genetics, Bologna, Italy; Department of Microbiology and Immunology, Brody School of Medicine, East Carolina University, Greenville, NC, United States (literal)

Titolo

PLC-beta 1 regulates the expression of miR-210 during mithramycin-mediated erythroid differentiation in K562 cells (literal)

Abstract

PLC-beta 1 (PLC?1) inhibits in human K562 cells erythroid differentiation induced by mithramycin (MTH) by targeting miR-210 expression. Inhibition of miR-210 affects the erythroid differentiation pathway and it occurs to a greater extent in MTH-treated cells. Overexpression of PLC?1 suppresses the differentiation of K562 elicited by MTH as demonstrated by the absence of ?-globin expression. Inhibition of PLC?1 expression is capable to promote the differentiation process leading to a recovery of ?-globin gene even in the absence of MTH. Our experimental evidences suggest that PLC?1 signaling regulates erythropoiesis through miR-210. Indeed overexpression of PLC?1 leads to a decrease of miR-210 expression after MTH treatment. Moreover miR-210 is up-regulated when PLC?1 expression is down-regulated. When we silenced PKC? by RNAi technique, we found a decrease in miR-210 and ?-globin expression levels, which led to a severe slowdown of cell differentiation in K562 cells and these effects were the same encountered in cells overexpressing PLC?1. Therefore we suggest a novel role for PLC?1 in regulating miR-210 and our data hint at the fact that, in human K562 erythroleukemia cells, the modulation of PLC?1 expression is able to exert an impairment of normal erythropoiesis as assessed by ?-globin expression. (literal)

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