Evidence map›Paper›PMID 21297667›Full record

ArticleOncogene2011

Targeting SET/I(2)PP2A oncoprotein functions as a multi-pathway strategy for cancer therapy.

C H Switzer, R Y S Cheng, T M Vitek, D J Christensen, D A Wink, M P Vitek

Abstract read
In one paragraph

Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed
6.7field-weighted citation impact, top 2% 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

92 citing papers in PubMed, 169 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Targeting PP2A in cancer: an underrated option.Journal of experimental & clinical cancer research : CR · 2025
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Circular MTHFD2L RNA-encoded CM-248aa inhibits gastric cancer progression by targeting the SET-PP2A interaction.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
  15. A direct interaction between RhoGDIα/Tau alleviates hyperphosphorylation of Tau in Alzheimer's disease and vascular dementia.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2023
    Article
  16. Article
  17. The SET oncoprotein promotes estrogen-induced transcription by facilitating establishment of active chromatin.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  18. Review
  19. Article
  20. Article

32 more citing papers are in PubMed but not listed here.

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

6 authors at 4 institutions in 1 country.

C H SwitzerRadiation Biology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
R Y S Cheng
T M Vitek
D J Christensen
D A Wink
M P Vitek
National Cancer Institute · USNational Institutes of Health · USResearch Triangle Park Foundation · USTriangle · US

Funding

Nitric Oxide as a Modifier of Oxidative StressZIASC007281 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI WINK, DAVID · 2009 to 2025
$8.1M
Properties of redox modified NSAIDs in cancer prevention and treatmentZIABC010899 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WINK, DAVID · 2009 to 2025
$6.7M
Intramural NIH HHS ZIA BC010899Intramural NIH HHS ZIA SC007281
6 · The paper itself

Abstract

The SET oncoprotein participates in cancer progression by affecting multiple cellular processes, inhibiting the tumor suppressor protein phosphatase 2A (PP2A), and inhibiting the metastasis suppressor nm23-H1. On the basis of these multiple activities, we hypothesized that targeted inhibition of SET would have multiple discrete and measurable effects on cancer cells. Here, the effects of inhibiting SET oncoprotein function on intracellular signaling and proliferation of human cancer cell lines was investigated. We observed the effects of COG112, a novel SET interacting peptide, on PP2A activity, Akt signaling, nm23-H1 activity and cellular migration/invasion in human U87 glioblastoma and MDA-MB-231 breast adenocarcinoma cancer cell lines. We found that COG112 interacted with SET protein and inhibited the association between SET and PP2A catalytic subunit (PP2A-c) and nm23-H1. The interaction between COG112 and SET caused PP2A phosphatase and nm23-H1 exonuclease activities to increase. COG112-mediated increases in PP2A activity resulted in the inhibition of Akt signaling and cellular proliferation. Additionally, COG112 inhibited SET association with Ras-related C(3) botulinum toxin substrate 1 (Rac1), leading to decreased cellular migration and invasion. COG112 treatment releases the SET-mediated inhibition of the tumor suppressor PP2A, as well as the metastasis suppressor nm23-H1. These results establish SET as a novel molecular target and that the inhibition of SET may have beneficial effects in cancer chemotherapy.

Indexed as

Antineoplastic AgentsCell Line, TumorCell MovementCell ProliferationDNA-Binding ProteinsHistone ChaperonesHumansNeoplasmsNM23 Nucleoside Diphosphate KinasesPeptidesProto-Oncogene Proteins c-aktrac1 GTP-Binding ProteinSignal TransductionTranscription FactorsAntineoplastic AgentsCOG112 peptideDNA-Binding ProteinsHistone ChaperonesNM23 Nucleoside Diphosphate KinasesNME1 protein, humanPeptidesProto-Oncogene Proteins c-aktrac1 GTP-Binding ProteinRAC1 protein, humanSET protein, humanTranscription Factors

Identifiers

PMID21297667
PMCPMC3107340
OpenAlexW2021359328

What OpenQuestion holds

Textmetadata
LicenceTDM
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.