Evidence map›Paper›PMID 19435914›Full record

ArticleCancer research2009

NORE1A tumor suppressor candidate modulates p21CIP1 via p53.

Diego F Calvisi, Howard Donninger, Michele D Vos, Michael J Birrer, Laura Gordon, Virna Leaner, Geoffrey J Clark

Open access · hybridAbstract read
In one paragraph

Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

34 citing papers in PubMed, 65 citations in OpenAlex.

  1. NORE1A loss promotes MASLD/MASH.Transgenic research · 2024
    Article
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  7. Review
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  11. Review
  12. Article
  13. Ras signaling through RASSF proteins.Seminars in cell & developmental biology · 2016
    Review
  14. Nore1a drives Ras to flick the P53 senescence switch.Molecular & cellular oncology · 2016
    Article
  15. Article
  16. Article
  17. Ras Regulates Rb via NORE1A.The Journal of biological chemistry · 2016
    Article
  18. Article
  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

7 authors at 4 institutions in 3 countries.

Diego F CalvisiInstitut für Pathologie, Ernst-Moritz-Arndt-Universität, Greifswald, Germany.
Howard Donninger
Michele D Vos
Michael J Birrer
Laura Gordon
Virna Leaner
Geoffrey J Clark
University of Louisville · USNational Cancer Institute · USUniversität Greifswald · DEUniversity of Cape Town · ZA

Funding

PROJ 12: STEM CELL-BASED VACCINE FOR CANCER PROPHYLAXISP20RR018733 · NCRR · UNIVERSITY OF LOUISVILLE · PI TRENT, JOHN O · 2003 to 2011
$18.9M
USE OF TRANSCRIPTIONAL FACTORS AS TARGETS AND AGENTS IN CARCINOGENESISZ01SC000165 · SC · DIVISION OF CLINICAL SCIENCES - NCI · PI BIRRER, MICHAEL · 1996 to 2008
$974k
The Use of Transcriptional Factors as Targets and Agents in CarcinogenesisZIASC000165 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI BIRRER, MICHAEL · 2009 to 2009
$187k
THE MOLECULAR MECHANISMS OF ONCOGENE ACTIONZ01SC000164 · SC · CLINICAL SCIENCES · PI BIRRER, MICHAEL · 1996 to 2006
–
Intramural NIH HHS Z01 SC000164Intramural NIH HHS Z01 SC000165NCRR NIH HHS P20 RR018733NCRR NIH HHS RR18733
6 · The paper itself

Abstract

NORE1A (RASSF5) is a proapoptotic Ras effector that is frequently inactivated by promoter methylation in human tumors. It is structurally related to the RASSF1A tumor suppressor and is itself implicated as a tumor suppressor. In the presence of activated Ras, NORE1A is a potent inducer of apoptosis. However, when expressed at lower levels in the absence of activated Ras, NORE1A seems to promote cell cycle arrest rather than apoptosis. The mechanisms underlying NORE1A action are poorly understood. We have used microarray analysis of an inducible NORE1A system to screen for physiologic signaling targets of NORE1A action. Using this approach, we have identified several potential signaling pathways modulated by NORE1A. In particular, we identify the cyclin-dependent kinase inhibitor p21(CIP1) as a target for NORE1A activation and show that it is a vital component of NORE1A-mediated growth inhibition. In primary human hepatocellular carcinomas (HCC), loss of NORE1A expression is frequent and correlates tightly with loss of p21(CIP1) expression. NORE1A down-regulation in HCC also correlates with poor prognosis, enhanced proliferation, survival, and angiogenic tumor characteristics. Experimental inactivation of NORE1A results in the loss of p21(CIP1) expression and promotes proliferation. The best characterized activator of p21(CIP1) is the p53 master tumor suppressor. Further experiments showed that NORE1A activates p21(CIP1) via promoting p53 nuclear localization. Thus, we define the molecular basis of NORE1A-mediated growth inhibition and implicate NORE1A as a potential component of the ill-defined connection between Ras and p53.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsApoptosis Regulatory ProteinsCarcinoma, HepatocellularCell AdhesionCell ProliferationCells, CulturedCell SurvivalCyclin-Dependent Kinase Inhibitor p21Gene Expression RegulationGene Expression Regulation, NeoplasticGenes, Tumor SuppressorHCT116 CellsHumansLiver NeoplasmsMiceAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21Monomeric GTP-Binding ProteinsRASSF5 protein, humanRNA, Small InterferingTumor Suppressor Protein p53

Identifiers

PMID19435914
PMCPMC6957251
OpenAlexW2044182002

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.