Evidence map›Paper›PMID 15684389›Full record

ArticleMolecular and cellular biology2005

Nm23-H1 metastasis suppressor expression level influences the binding properties, stability, and function of the kinase suppressor of Ras1 (KSR1) Erk scaffold in breast carcinoma cells.

Massimiliano Salerno, Diane Palmieri, Amina Bouadis, Douglas Halverson, Patricia S Steeg

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

43 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. NME/NM23/NDPK and Histidine Phosphorylation.International journal of molecular sciences · 2020
    Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Modulation of small GTPase activity by NME proteins.Laboratory investigation; a journal of technical methods and pathology · 2018
    Review
  11. The NDPK/NME superfamily: state of the art.Laboratory investigation; a journal of technical methods and pathology · 2018
    Article
  12. Metastasis suppressors: functional pathways.Laboratory investigation; a journal of technical methods and pathology · 2018
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Regulation of the metastasis suppressor Nm23-H1 by tumor viruses.Naunyn-Schmiedeberg's archives of pharmacology · 2015
    Review
  19. Article
  20. 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.

Massimiliano SalernoWomen's Cancers Section, Laboratory of Pathology, Building 10, Room 2A33, National Cancer Institute, Bethesda, MD 20892, USA. maxsal@mail.nih.gov
Diane Palmieri
Amina Bouadis
Douglas Halverson
Patricia S Steeg
Center for Cancer Research · USNational Institutes of Health · US

Funding

Molecular Biology of the Metastatic PhenotypeZIASC000892 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI STEEG, PATRICIA SCHRIVER · 2009 to 2023
$8.4M
MOLECULAR BIOLOGY OF THE METASTATIC PHENOTYPEZ01SC000892 · SC · DIVISION OF CLINICAL SCIENCES - NCI · PI STEEG, PATRICIA SCHRIVER · 1996 to 2008
$1.3M
6 · The paper itself

Abstract

Metastatic disease is a significant contributor to cancer patient mortality. We previously reported that the Kinase Suppressor of Ras1 (KSR1) scaffold protein for the Erk mitogen-activated protein kinase pathway coimmunoprecipitated the metastasis suppressor protein Nm23-H1. We now hypothesize that altered expression levels of Nm23-H1 influence the binding properties, stability, and function of the KSR1 scaffold. Increased coimmunoprecipitation of Hsp90 with KSR1 was observed in either stable or transient transfectants of nm23-H1 in MDA-MB-435 human breast carcinoma cells. Similar trends were also observed in the cytoplasmic and nuclear fractions of cells. Cells expressing high levels of Nm23-H1 exhibited increased KSR1 degradation in the presence of either cycloheximide or an Hsp90-directed drug currently in clinical trial, 17-allylamino-17-demethoxygeldanamycin (17-AAG). In agreement with KSR1 degradation data, high-Nm23-H1-expression cells were preferentially inhibited in anchorage-independent colonization assays by 17-AAG. KSR1 scaffold binding patterns are dynamic in both the cytoplasmic and nuclear compartments, modulated by metastasis suppressor expression. Metastasis suppressor expression levels can impact traditional signaling pathways, such as the Erk pathway, resulting in altered tumor cell sensitivity to cancer therapeutics.

Indexed as

BenzoquinonesBreast NeoplasmsCell FractionationCell NucleusCell ProliferationCycloheximideCytoplasmExtracellular Signal-Regulated MAP KinasesFemaleGenes, Tumor SuppressorHSP90 Heat-Shock ProteinsHumansLactams, MacrocyclicNM23 Nucleoside Diphosphate KinasesNucleoside-Diphosphate KinaseProtein BindingBenzoquinonesCycloheximideExtracellular Signal-Regulated MAP KinasesHSP90 Heat-Shock ProteinsKSR-1 protein kinaseLactams, MacrocyclicNM23 Nucleoside Diphosphate KinasesNME1 protein, humanNucleoside-Diphosphate KinaseProtein Kinase InhibitorsProtein KinasesRifabutintanespimycin

Identifiers

PMID15684389
PMCPMC548014
OpenAlexW2094454350

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.