Evidence map›Paper›PMID 33810430›Full record

ArticleMetabolites2021

Pemetrexed Hinders Translation Inhibition upon Low Glucose in Non-Small Cell Lung Cancer Cells.

Marie Piecyk, Mouna Triki, Pierre-Alexandre Laval, Helena Dragic, Laura Cussonneau, Joelle Fauvre, Cédric Duret, Nicolas Aznar, Toufic Renno, Serge N Manié and 2 more

Open access · goldAbstract read
In one paragraph

Article in Metabolites, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 49% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
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

12 authors at 3 institutions in 1 country.

Marie PiecykUniversité Lyon, Cancer Research Centre of Lyon, INSERM 1052, CNRS 5286, F-69008 Lyon, France.
Mouna TrikiUniversité Lyon, Cancer Research Centre of Lyon, INSERM 1052, CNRS 5286, F-69008 Lyon, France.
Pierre-Alexandre LavalUniversité Lyon, Cancer Research Centre of Lyon, INSERM 1052, CNRS 5286, F-69008 Lyon, France.
Helena DragicUniversité Lyon, Cancer Research Centre of Lyon, INSERM 1052, CNRS 5286, F-69008 Lyon, France.
Laura CussonneauUniversité Clermont Auvergne, INRAE, Unité de Nutrition Humaine, UMR1019, 63122 Clermont-Ferrand, France.ORCID 0000-0002-3017-2685
Joelle FauvreUniversité Lyon, Cancer Research Centre of Lyon, INSERM 1052, CNRS 5286, F-69008 Lyon, France.
Cédric DuretUniversité Lyon, Cancer Research Centre of Lyon, INSERM 1052, CNRS 5286, F-69008 Lyon, France.ORCID 0000-0003-1769-8081
Nicolas AznarUniversité Lyon, Cancer Research Centre of Lyon, INSERM 1052, CNRS 5286, F-69008 Lyon, France.ORCID 0000-0003-3338-9932
Toufic RennoUniversité Lyon, Cancer Research Centre of Lyon, INSERM 1052, CNRS 5286, F-69008 Lyon, France.
Serge N ManiéInserm U1242, Université de Rennes, Centre de Lutte Contre le Cancer Eugène Marquis, 35042 Rennes, France.
Cédric ChaverouxUniversité Lyon, Cancer Research Centre of Lyon, INSERM 1052, CNRS 5286, F-69008 Lyon, France.ORCID 0000-0002-4116-3354
Carole Ferraro-PeyretUniversité Lyon, Cancer Research Centre of Lyon, INSERM 1052, CNRS 5286, F-69008 Lyon, France.
Université Claude Bernard Lyon 1 · FRInserm · FRUniversité Clermont Auvergne · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genetic alterations in non-small cell lung cancers (NSCLC) stimulate the generation of energy and biomass to promote tumor development. However, the efficacy of the translation process is finely regulated by stress sensors, themselves often controlled by nutrient availability and chemotoxic agents. Yet, the crosstalk between therapeutic treatment and glucose availability on cell mass generation remains understudied. Herein, we investigated the impact of pemetrexed (PEM) treatment, a first-line agent for NSCLC, on protein synthesis, depending on high or low glucose availability. PEM treatment drastically repressed cell mass and translation when glucose was abundant. Surprisingly, inhibition of protein synthesis caused by low glucose levels was partially dampened upon co-treatment with PEM. Moreover, PEM counteracted the elevation of the endoplasmic reticulum stress (ERS) signal produced upon low glucose availability, providing a molecular explanation for the differential impact of the drug on translation according to glucose levels. Collectively, these data indicate that the ERS constitutes a molecular crosstalk between microenvironmental stressors, contributing to translation reprogramming and proteostasis plasticity.

Indexed as

ER stress signalingglucose availabilityNSCLCpemetrexedprotein synthesis

Identifiers

PMID33810430
PMCPMC8067050
OpenAlexW3148834397

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.