Evidence map›Paper›PMID 24764298›Full record

ArticleThe Journal of biological chemistry2014

Enhanced arginine methylation of programmed cell death 4 protein during nutrient deprivation promotes tumor cell viability.

Marta M Fay, James M Clegg, Kimberly A Uchida, Matthew A Powers, Katharine S Ullman

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 22% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. The Impact of Pdcd4, a Translation Inhibitor, on Drug Resistance.Pharmaceuticals (Basel, Switzerland) · 2024
    Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Control Mechanisms of the Tumor Suppressor PDCD4: Expression and Functions.International journal of molecular sciences · 2019
    Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. 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

5 authors at 2 institutions in 1 country.

Marta M FayFrom the Oncological Sciences Department, Huntsman Cancer Institute and.
James M CleggFrom the Oncological Sciences Department, Huntsman Cancer Institute and.
Kimberly A UchidaFrom the Oncological Sciences Department, Huntsman Cancer Institute and Department of Bioengineering, University of Utah, Salt Lake City, Utah 84112.
Matthew A PowersFrom the Oncological Sciences Department, Huntsman Cancer Institute and.
Katharine S UllmanFrom the Oncological Sciences Department, Huntsman Cancer Institute and katie.ullman@hci.utah.edu.
Huntsman Cancer Institute · USUniversity of Utah · US

Funding

UTAH REGIONAL CANCER CENTERP30CA042014 · NCI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Jared P Rutter · 1986 to 2026
$72.6M
Capitalizing on a New Biomarker Signature for Cancer PrognosisR21CA173064 · NCI · UNIVERSITY OF UTAH · PI ULLMAN, KATHARINE S · 2013 to 2014
$352k
NCI NIH HHS P30 CA042014NCI NIH HHS R21 CA173064
6 · The paper itself

Abstract

The role of programmed cell death 4 (PDCD4) in tumor biology is context-dependent. PDCD4 is described as a tumor suppressor, but its coexpression with protein arginine methyltransferase 5 (PRMT5) promotes accelerated tumor growth. Here, we report that PDCD4 is methylated during nutrient deprivation. Methylation occurs because of increased stability of PDCD4 protein as well as increased activity of PRMT5 toward PDCD4. During nutrient deprivation, levels of methylated PDCD4 promote cell viability, which is dependent on an enhanced interaction with eIF4A. Upon recovery from nutrient deprivation, levels of methylated PDCD4 are regulated by phosphorylation, which controls both the localization and stability of methylated PDCD4. This study reveals that, in response to particular environmental cues, the role of PDCD4 is up-regulated and is advantageous for cell viability. These findings suggest that the methylated form of PDCD4 promotes tumor viability during nutrient deprivation, ultimately allowing the tumor to grow more aggressively.

Indexed as

Gene Expression Regulation, NeoplasticApoptosis Regulatory ProteinsArginineCell Line, TumorCell SurvivalHumansMethylationNeoplasm ProteinsNeoplasmsPhosphorylationProtein-Arginine N-MethyltransferasesRNA-Binding ProteinsUp-RegulationApoptosis Regulatory ProteinsArginineNeoplasm ProteinsPDCD4 protein, humanPRMT5 protein, humanProtein-Arginine N-MethyltransferasesRNA-Binding ProteinseIF4AMolecular Cell BiologyNutrient DeprivationOncogenePDCD4PRMT5Protein MethylationTranslation Initiation FactorTumor Cell BiologyTumor Suppressor Gene

Identifiers

PMID24764298
PMCPMC4067190
OpenAlexW2093821263

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.