Evidence map›Paper›PMID 23300087›Full record

ArticleThe Journal of biological chemistry2013

Reprogramming of the microRNA transcriptome mediates resistance to rapamycin.

Hana Totary-Jain, Despina Sanoudou, Iddo Z Ben-Dov, Cula N Dautriche, Paolo Guarnieri, Steven O Marx, Thomas Tuschl, Andrew R Marks

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

33 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
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  7. Decreased LIN28B in preeclampsia impairs human trophoblast differentiation and migration.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  8. Review
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  15. Emerging Role of MicroRNAs in mTOR Signaling.Cellular and molecular life sciences : CMLS · 2017
    Review
  16. mTOR inhibitors in urinary bladder cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Review
  17. Review
  18. Article
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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

8 authors at 4 institutions in 2 countries.

Hana Totary-JainDepartment of Physiology and Cellular Biophysics, the Clyde and Helen Wu Center for Molecular Cardiology, Columbia University, New York, New York 10032, USA. ht2167@columbia.edu
Despina Sanoudou
Iddo Z Ben-Dov
Cula N Dautriche
Paolo Guarnieri
Steven O Marx
Thomas Tuschl
Andrew R Marks
Columbia University · USRockefeller University · USHerbert Irving Comprehensive Cancer CenterNational and Kapodistrian University of Athens · GR

Funding

MicroRNA Detargeting Novel Therapy for Coronary Artery DiseaseK99HL109133 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TOTARY-JAIN, HANA · 2011 to 2012
$268k
Regulation of Vascular Smooth Muscle Cell ProliferationF32HL088815 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TOTARY-JAIN, HANA · 2008 to 2010
$158k
Howard Hughes Medical InstituteNHLBI NIH HHS F32 HL088815NHLBI NIH HHS F32HL088815NHLBI NIH HHS K99 HL109133NHLBI NIH HHS K99HL109133
6 · The paper itself

Abstract

The mammalian target of rapamycin (mTOR) is a central regulator of cell proliferation that is often deregulated in cancer. Inhibitors of mTOR, including rapamycin and its analogues, are being evaluated as antitumor agents. For their promise to be fulfilled, it is of paramount importance to identify the mechanisms of resistance and develop novel therapies to overcome it. Given the emerging role of microRNAs (miRNAs) in tumorigenesis, we hypothesized that miRNAs could play important roles in the response of tumors to mTOR inhibitors. Long-term rapamycin treatment showed extensive reprogramming of miRNA expression, characterized by up-regulation of miR-17-92 and related clusters and down-regulation of tumor suppressor miRNAs. Inhibition of members of the miR-17-92 clusters or delivery of tumor suppressor miRNAs restored sensitivity to rapamycin. This study identifies miRNAs as new downstream components of the mTOR-signaling pathway, which may determine the response of tumors to mTOR inhibitors. It also identifies potential markers to assess the efficacy of treatment and provides novel therapeutic targets to treat rapamycin-resistant tumors.

Indexed as

AnimalsAntibiotics, AntineoplasticCell Line, TumorDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticMiceMicroRNAsNeoplasm ProteinsRNA, NeoplasmSignal TransductionSirolimusTime FactorsTOR Serine-Threonine KinasesTranscriptomeAntibiotics, AntineoplasticMicroRNAsMIRN17-92 microRNA, mousemTOR protein, mouseNeoplasm ProteinsRNA, NeoplasmSirolimusTOR Serine-Threonine Kinases

Identifiers

PMID23300087
PMCPMC3585042
OpenAlexW1988061615

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.