Evidence map›Paper›PMID 20885442›Full record

ArticleCell death and differentiation2011

miR-210 is overexpressed in late stages of lung cancer and mediates mitochondrial alterations associated with modulation of HIF-1 activity.

M-P Puisségur, N M Mazure, T Bertero, L Pradelli, S Grosso, K Robbe-Sermesant, T Maurin, K Lebrigand, B Cardinaud, V Hofman and 8 more

Open access · hybridAbstract read
In one paragraph

Article in Cell death and differentiation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 240 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
240citing papers in PubMed, 7 pooled it
10.4field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

240 citing papers in PubMed, 7 syntheses or guidelines pooled it, 411 citations in OpenAlex.

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180 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

18 authors at 7 institutions in 2 countries.

M-P PuisségurInstitut de Pharmacologie Moléculaire et Cellulaire, CNRS UMR6097, Sophia Antipolis, France.
N M Mazure
T Bertero
L Pradelli
S Grosso
K Robbe-Sermesant
T Maurin
K Lebrigand
B Cardinaud
V Hofman
S Fourre
V Magnone
J E Ricci
J Pouysségur
P Gounon
P Hofman
P Barbry
B Mari
Université Côte d'Azur · FRCentre National de la Recherche Scientifique · FRCentre Hospitalier Universitaire de Nice · FRInstitut de Pharmacologie Moléculaire et Cellulaire · FRCentre Antoine Lacassagne · FRCentre Méditerranéen de Médecine Moléculaire · FRMemorial Sloan Kettering Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Following the identification of a set of hypoxia-regulated microRNAs (miRNAs), recent studies have highlighted the importance of miR-210 and of its transcriptional regulation by the transcription factor hypoxia-inducible factor-1 (HIF-1). We report here that miR-210 is overexpressed at late stages of non-small cell lung cancer. Expression of miR-210 in lung adenocarcinoma A549 cells caused an alteration of cell viability associated with induction of caspase-3/7 activity. miR-210 induced a loss of mitochondrial membrane potential and the apparition of an aberrant mitochondrial phenotype. The expression profiling of cells overexpressing miR-210 revealed a specific signature characterized by enrichment for transcripts related to 'cell death' and 'mitochondrial dysfunction', including several subunits of the electron transport chain (ETC) complexes I and II. The transcript coding for one of these ETC components, SDHD, subunit D of succinate dehydrogenase complex (SDH), was validated as a bona fide miR-210 target. Moreover, SDHD knockdown mimicked miR-210-mediated mitochondrial alterations. Finally, miR-210-dependent targeting of SDHD was able to activate HIF-1, in line with previous studies linking loss-of-function SDH mutations to HIF-1 activation. miR-210 can thus regulate mitochondrial function by targeting key ETC component genes with important consequences on cell metabolism, survival and modulation of HIF-1 activity. These observations help explain contradictory data regarding miR-210 expression and its putative function in solid tumors.

Indexed as

ApoptosisCarcinoma, Non-Small-Cell LungCaspase 3Caspase 7Cell HypoxiaCell Line, TumorCell SurvivalDown-RegulationGene Expression ProfilingGene Expression Regulation, NeoplasticHumansHypoxia-Inducible Factor 1, alpha SubunitLung NeoplasmsMicroRNAsMitochondriaMitochondrial ProteinsCaspase 3Caspase 7HIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitMicroRNAsMIRN210 microRNA, humanMitochondrial ProteinsRNA, MessengerRNA, Small InterferingSuccinate Dehydrogenase

Identifiers

PMID20885442
PMCPMC3131992
OpenAlexW2044662583

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.