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Int. J. Mol. Sci. 2017, 18(10), 2167; doi:10.3390/ijms18102167

Ferritin Heavy Subunit Silencing Blocks the Erythroid Commitment of K562 Cells via miR-150 up-Regulation and GATA-1 Repression

1
Research Center of Advanced Biochemistry and Molecular Biology, Department of Experimental and Clinical Medicine, University Magna Græcia, 88100 Catanzaro, Italy
2
Laboratory of Molecular Haematopoiesis and Stem Cell Biology, Department of Experimental and Clinical Medicine, University Magna Græcia, 88100 Catanzaro, Italy
3
Department of Experimental and Clinical Medicine, University of Catanzaro “Magna Graecia”, 88100 Catanzaro, Italy
These authors contributed equally to this work.
*
Author to whom correspondence should be addressed.
Received: 11 September 2017 / Revised: 9 October 2017 / Accepted: 12 October 2017 / Published: 17 October 2017
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Abstract

Erythroid differentiation is a complex and multistep process during which an adequate supply of iron for hemoglobinization is required. The role of ferritin heavy subunit, in this process, has been mainly attributed to its capacity to maintain iron in a non-toxic form. We propose a new role for ferritin heavy subunit (FHC) in controlling the erythroid commitment of K562 erythro-myeloid cells. FHC knockdown induces a change in the balance of GATA transcription factors and significantly reduces the expression of a repertoire of erythroid-specific genes, including α- and γ-globins, as well as CD71 and CD235a surface markers, in the absence of differentiation stimuli. These molecular changes are also reflected at the morphological level. Moreover, the ability of FHC-silenced K562 cells to respond to the erythroid-specific inducer hemin is almost completely abolished. Interestingly, we found that this new role for FHC is largely mediated via regulation of miR-150, one of the main microRNA implicated in the cell-fate choice of common erythroid/megakaryocytic progenitors. These findings shed further insight into the biological properties of FHCand delineate a role in erythroid differentiation where this protein does not act as a mere iron metabolism-related factor but also as a critical regulator of the expression of genes of central relevance for erythropoiesis. View Full-Text
Keywords: ferritin heavy subunit; differentiation; K562; miR-150; GATA-1 ferritin heavy subunit; differentiation; K562; miR-150; GATA-1
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Zolea, F.; Battaglia, A.M.; Chiarella, E.; Malanga, D.; Marco, C.D.; Bond, H.M.; Morrone, G.; Costanzo, F.; Biamonte, F. Ferritin Heavy Subunit Silencing Blocks the Erythroid Commitment of K562 Cells via miR-150 up-Regulation and GATA-1 Repression. Int. J. Mol. Sci. 2017, 18, 2167.

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