Evidence map›Paper›PMID 17355970›Full record

ArticleThe Journal of biological chemistry2007

Activation of a novel calcineurin-mediated insulin-like growth factor-1 receptor pathway, altered metabolism, and tumor cell invasion in cells subjected to mitochondrial respiratory stress.

Manti Guha, Satish Srinivasan, Gopa Biswas, Narayan G Avadhani

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

39 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Mitochondrial DNA variation and cancer.Nature reviews. Cancer · 2021
    Review
  5. Review
  6. Article
  7. Esophageal 3D organoids ofOncotarget · 2019
    Article
  8. Review
  9. Article
  10. Review
  11. Article
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  13. Review
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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

4 authors at 1 institution in 1 country.

Manti GuhaDepartment of Animal Biology and the Mari Lowe Center for Comparative Oncology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
Satish Srinivasan
Gopa Biswas
Narayan G Avadhani
University of Pennsylvania · US

Funding

Role of Mitochondrial Respiratory Stress Signaling in Cancer ProgressionR01CA022762 · NCI · UNIVERSITY OF PENNSYLVANIA · PI AVADHANI, NARAYAN G · 1985 to 2013
$3.3M
MITOCHONDRIAL D-LOOP DNA MUTATIONS AND GENE EXPRESSIONR37CA022762 · NCI · UNIVERSITY OF PENNSYLVANIA · PI AVADHANI, NARAYAN G · 1994 to 2002
$299k
NCI NIH HHS CA22762NCI NIH HHS R01 CA022762NCI NIH HHS R37 CA022762
6 · The paper itself

Abstract

We have previously shown that disruption of mitochondrial membrane potential by depletion of mitochondrial DNA (mtDNA) or treatment with a mitochondrial ionophore, carbonyl cyanide m-chlorophenylhydrazone, initiates a stress signaling, which causes resistance to apoptosis, and induces invasive behavior in C2C12 myocytes and A549 cells. In the present study we show that calcineurin (Cn), activated as part of this stress signaling, plays an important role in increased glucose uptake and glycolysis. Here we report that, although both insulin and insulin-like growth factor-1 receptor levels (IR and IGF1R, respectively) are increased in response to mitochondrial stress, autophosphorylation of IGF1R was selectively increased suggesting a shift in receptor pathways. Using an approach with FK506, an inhibitor of Cn, and mRNA silencing by small interference RNA we show that mitochondrial stress-activated Cn is critical for increased GLUT 4 and IGF1R expression and activation. The importance of the IGF1R pathway in cell survival under mitochondrial stress is demonstrated by increased apoptosis either by IGF1R mRNA silencing or by treatment with IGF1R inhibitors (AG1024 and picropodophyllin). This study describes a novel mechanism of mitochondrial stress-induced metabolic shift involving Cn with implications in resistance to apoptosis and tumor proliferation.

Indexed as

Oxidative StressSignal TransductionAdenosine TriphosphateAnimalsApoptosisCalcineurinCalcium SignalingCell MembraneCell RespirationCells, CulturedDeoxyglucoseGlucose Transporter Type 4HumansImmunoblottingImmunoprecipitationLung NeoplasmsAdenosine TriphosphateCalcineurinDeoxyglucoseGlucose Transporter Type 4Receptor, IGF Type 1Receptor, InsulinRNA, MessengerRNA, Small Interfering

Identifiers

PMID17355970
PMCPMC3800738
OpenAlexW2071661441

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.