Evidence map›Paper›PMID 24444362›Full record

ArticleAntioxidants & redox signaling2014

MicroRNA-126 suppresses mesothelioma malignancy by targeting IRS1 and interfering with the mitochondrial function.

Marco Tomasetti, Linda Nocchi, Sara Staffolani, Nicola Manzella, Monica Amati, Jacob Goodwin, Katarina Kluckova, Maria Nguyen, Elisabetta Strafella, Martina Bajzikova and 7 more

Abstract read
In one paragraph

Article in Antioxidants & redox signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 5% 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

57 citing papers in PubMed, 1 synthesis or guideline pooled it, 90 citations in OpenAlex.

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  6. MicroRNA-126 (MiR-126): key roles in related diseases.Journal of physiology and biochemistry · 2024
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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

17 authors at 4 institutions in 5 countries.

Marco Tomasetti1 Department of Clinical and Molecular Science, Polytechnic University of Marche , Ancona, Italy .
Linda Nocchi
Sara Staffolani
Nicola Manzella
Monica Amati
Jacob Goodwin
Katarina Kluckova
Maria Nguyen
Elisabetta Strafella
Martina Bajzikova
Martin Peterka
Sandra Lettlova
Jaroslav Truksa
Wan Lee
Lan-Feng Dong
Lory Santarelli
Jiri Neuzil
Marche Polytechnic University · ITCzech Academy of Sciences · CZGriffith University · AUDongguk University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsMiR126 was found to be frequently lost in many types of cancer, including malignant mesothelioma (MM), which represents one of the most challenging neoplastic diseases. In this study, we investigated the potential tumor suppressor function of MiR126 in MM cells. The effect of MiR126 was examined in response to oxidative stress, aberrant mitochondrial function induced by inhibition of complex I, mitochondrial DNA (mtDNA) depletion, and hypoxia.

resultsMiR126 was up-regulated by oxidative stress in nonmalignant mesothelial (Met5A) and MM (H28) cell lines. In Met5A cells, rotenone inhibited MiR126 expression, but mtDNA depletion and hypoxia up-regulated MiR126. However, these various stimuli suppressed the levels of MiR126 in H28 cells. MiR126 affected mitochondrial energy metabolism, reduced mitochondrial respiration, and promoted glycolysis in H28 cells. This metabolic shift, associated with insulin receptor substrate-1 (IRS1)-modulated ATP-citrate lyase deregulation, resulted in higher ATP and citrate production. These changes were linked to the down-regulation of IRS1 by ectopic MiR126, reducing Akt signaling and inhibiting cytosolic sequestration of Forkhead box O1 (FoxO1), which promoted the expression of genes involved in gluconeogenesis and oxidative stress defense. These metabolic changes induced hypoxia-inducible factor-1α (HIF1α) stabilization. Consequently, MiR126 suppressed the malignancy of MM cells in vitro, a notion corroborated by the failure of H28(MiR126) cells to form tumors in nude mice. INNOVATION AND

conclusionMiR126 affects mitochondrial energy metabolism, resulting in MM tumor suppression. Since MM is a fatal neoplastic disease with a few therapeutic options, this finding is of potential translational importance.

Indexed as

AnimalsCell HypoxiaCell Line, TumorCell ProliferationForkhead Box Protein O1Forkhead Transcription FactorsGene Expression Regulation, NeoplasticGlycolysisHumansHypoxia-Inducible Factor 1, alpha SubunitInsulin Receptor Substrate ProteinsLung NeoplasmsMesotheliomaMesothelioma, MalignantMice, NudeMicroRNAsForkhead Box Protein O1Forkhead Transcription FactorsFOXO1 protein, humanHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitInsulin Receptor Substrate ProteinsIRS1 protein, humanMicroRNAsMIRN126 microRNA, human

Identifiers

PMID24444362
PMCPMC4215384
OpenAlexW2016818544

What OpenQuestion holds

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Registered trials

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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.