http://www.cnr.it/ontology/cnr/individuo/prodotto/ID282986
Downregulation of the mitochondrial calcium uniporter by cancer-related miR-25 (Articolo in rivista)
- Type
- Label
- Downregulation of the mitochondrial calcium uniporter by cancer-related miR-25 (Articolo in rivista) (literal)
- Anno
- 2013-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1016/j.cub.2012.11.026 (literal)
- Alternative label
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Marchi S.; Lupini L.; Patergnani S.; Rimessi A.; Missiroli S.; Bonora M.; Bononi A.; Corra F.; Giorgi C.; De Marchi E.; Poletti F.; Gafa R.; Lanza G.; Negrini M.; Rizzuto R.; Pinton P. (literal)
- Pagina inizio
- Pagina fine
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#url
- http://www.ncbi.nlm.nih.gov/pubmed/23246404 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
- Rivista
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo
- Note
- Scopu (literal)
- ISI Web of Science (WOS) (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- Department of Morphology, Surgery and Experimental Medicine, Interdisciplinary Center for the Study of Inflammation (ICSI), University of Ferrara, 44121 Ferrara, Italy; Department of Morphology, Surgery and Experimental Medicine, University of Ferrara, 44121 Ferrara, Italy; Anatomic Pathology Section, Department of Morphology, Surgery and Experimental Medicine, University of Ferrara, 44121 Ferrara, Italy; Department of Biomedical Sciences, University of Padua, CNR Neuroscience Institute, 35129 Padua, Italy (literal)
- Titolo
- Downregulation of the mitochondrial calcium uniporter by cancer-related miR-25 (literal)
- Abstract
- The recently discovered mitochondrial calcium uniporter
(MCU) promotes Ca2+ accumulation into the mitochondrial
matrix [1, 2]. We identified in silico miR-25 as a cancer-related
MCU-targeting microRNA family and demonstrate that its
overexpression in HeLa cells drastically reduces MCU levels
and mitochondrial Ca2+ uptake, while leaving other mitochondrial
parameters and cytosolic Ca2+ signals unaffected.
In human colon cancers and cancer-derived cells, miR-25
is overexpressed and MCU accordingly silenced. miR-25-
dependent reduction of mitochondrial Ca2+ uptake correlates
with resistance to apoptotic challenges and can
be reversed by anti-miR-25 overexpression. Overall, the
data demonstrate that microRNA targeting of mitochondrial
Ca2+ signaling favors cancer cell survival, thus providing
mechanistic insight into the role of mitochondria in
tumorigenesis and identifying a novel therapeutic target in
neoplasia. (literal)
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