Journal
GENE
Volume 657, Issue -, Pages 92-99Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.gene.2018.03.027
Keywords
Iron metabolism; Long non coding RNA; Reactive oxygen species
Categories
Funding
- Progetto ICaRe-Infrastruttura Calabrese per la medicina Rigenerativa: generazione di biobanche per la criopreservazione di cellule staminali umane e di tessuto osseo per use clinico e design e sviluppo di bioscaffold innovative [PON03PE_00009_2]
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Purpose: The heavy subunit of the iron storage protein ferritin (FHC) is essential for the intracellular iron metabolism and, at the same time, it represents a central hub of iron-independent pathways, such as cell proliferation, angiogenesis, p53 regulation, chemokine signalling, stem cell expansion, miRNAs expression. In this work we have explored the ability of FHC to modulate gene expression in K562 cells, through the up-regulation of the lncRNA H19 and its cognate miR-675. Materials and methods: Targeted silencing of FHC was performed by lentiviral-driven shRNA strategy. FHC reconstitution was obtained by full length FHC cDNA transfection with Lipofectamine 2000. ROS amounts were determined with the redox-sensitive probe H2DCFDA. H19, miR-675, miR-107, Twist1, ID3, EPHB6, GNS, ANK1 and SMAD6 mRNA amounts were quantified by Taqman assay and qPCR analysis. Results: FHC silencing in K562 cells modulates gene expression through the up-regulation of the lncRNA H19 and its cognate miR-675. Experimental findings demonstrate that the molecular mechanism underlying this phenomenon is represented by an FHC knock-down-triggered increase in reactive oxygen species (ROS) production. Conclusions: In this paper we uncover a so far not described function of the ferritin heavy subunit in the control of lncRNA pathways.
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