Evidence map›Paper›PMID 23492775›Full record

ArticleCell death & disease2013

MiR-210 promotes a hypoxic phenotype and increases radioresistance in human lung cancer cell lines.

S Grosso, J Doyen, S K Parks, T Bertero, A Paye, B Cardinaud, P Gounon, S Lacas-Gervais, A Noël, J Pouysségur and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
131citing papers in PubMed, 1 pooled it
10.1field-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

131 citing papers in PubMed, 1 synthesis or guideline pooled it, 212 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Hypoxia A Typical Target in Human Lung Cancer Therapy.Current protein & peptide science · 2024
    Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Extracellular RNA in melanoma: Advances, challenges, and opportunities.Frontiers in cell and developmental biology · 2023
    Review
  13. Review
  14. Review
  15. Article
  16. Skeletal muscle MiR-210 expression is associated with mitochondrial function in peripheral artery disease patients.Translational research : the journal of laboratory and clinical medicine · 2022
    Article
  17. Article
  18. Mitochondrial Epigenetics Regulating Inflammation in Cancer and Aging.Frontiers in cell and developmental biology · 2022
    Review
  19. Review
  20. Article

71 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

13 authors at 4 institutions in 2 countries.

S GrossoInstitut de Pharmacologie Moléculaire et Cellulaire (IPMC), Centre National de la Recherche Scientifique, CNRS UMR 7275, Sophia Antipolis, France.
J Doyen
S K Parks
T Bertero
A Paye
B Cardinaud
P Gounon
S Lacas-Gervais
A Noël
J Pouysségur
P Barbry
N M Mazure
B Mari
Inserm · FRUniversité Côte d'Azur · FRCentre National de la Recherche Scientifique · FRUniversity of Liège · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The resistance of hypoxic cells to radiotherapy and chemotherapy is a major problem in the treatment of cancer. Recently, an additional mode of hypoxia-inducible factor (HIF)-dependent transcriptional regulation, involving modulation of a specific set of micro RNAs (miRNAs), including miR-210, has emerged. We have recently shown that HIF-1 induction of miR-210 also stabilizes HIF-1 through a positive regulatory loop. Therefore, we hypothesized that by stabilizing HIF-1 in normoxia, miR-210 may protect cancer cells from radiation. We developed a non-small cell lung carcinoma (NSCLC)-derived cell line (A549) stably expressing miR-210 (pmiR-210) or a control miRNA (pmiR-Ctl). The miR-210-expressing cells showed a significant stabilization of HIF-1 associated with mitochondrial defects and a glycolytic phenotype. Cells were subjected to radiation levels ranging from 0 to 10 Gy in normoxia and hypoxia. Cells expressing miR-210 in normoxia had the same level of radioresistance as control cells in hypoxia. Under hypoxia, pmiR-210 cells showed a low mortality rate owing to a decrease in apoptosis, with an ability to grow even at 10 Gy. This miR-210 phenotype was reproduced in another NSCLC cell line (H1975) and in HeLa cells. We have established that radioresistance was independent of p53 and cell cycle status. In addition, we have shown that genomic double-strand breaks (DSBs) foci disappear faster in pmiR-210 than in pmiR-Ctl cells, suggesting that miR-210 expression promotes a more efficient DSB repair. Finally, HIF-1 invalidation in pmiR-210 cells removed the radioresistant phenotype, showing that this mechanism is dependent on HIF-1. In conclusion, miR-210 appears to be a component of the radioresistance of hypoxic cancer cells. Given the high stability of most miRNAs, this advantage could be used by tumor cells in conditions where reoxygenation has occurred and suggests that strategies targeting miR-210 could enhance tumor radiosensitization.

Indexed as

ApoptosisCarcinoma, Non-Small-Cell LungCell HypoxiaCell Line, TumorDNA Breaks, Double-StrandedDNA RepairGamma RaysGene Expression Regulation, NeoplasticHumansHypoxiaHypoxia-Inducible Factor 1Lung NeoplasmsMicroRNAsMitochondriaRadiation ToleranceSignal TransductionHypoxia-Inducible Factor 1MicroRNAsMIRN210 microRNA, human

Identifiers

PMID23492775
PMCPMC3615727
OpenAlexW2024139498

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.