Evidence map›Paper›PMID 28455242›Full record

ReviewCancer letters2017

The role of the NORE1A tumor suppressor in Oncogene-Induced Senescence.

Thibaut Barnoud, M Lee Schmidt, Howard Donninger, Geoffrey J Clark

Open access · greenAbstract readReview
In one paragraph

Review in Cancer letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

9 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. The Paradoxical Role of Cellular Senescence in Cancer.Frontiers in cell and developmental biology · 2021
    Review
  7. Review
  8. Review
  9. Review
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

4 authors at 2 institutions in 1 country.

Thibaut BarnoudProgram in Molecular and Cellular Oncogenesis, The Wistar Institute, Philadelphia PA 19104, USA.
M Lee SchmidtDepartment of Pharmacology and Toxicology, University of Louisville, KY 40202, USA.
Howard DonningerDepartment of Medicine, University of Louisville, KY 40202, USA.
Geoffrey J ClarkDepartment of Pharmacology and Toxicology, University of Louisville, KY 40202, USA. Electronic address: gjclar01@louisville.edu.
University of Louisville · USThe Wistar Institute · US

Funding

TRAINING PROGRAM IN BASIC CANCER RESEARCHT32CA009171 · NCI · WISTAR INSTITUTE · PI Alessandro Gardini · 1985 to 2026
$15.3M
The role of the Ras effector Nore1a in tumor suppressionR01CA133171 · NCI · UNIVERSITY OF LOUISVILLE · PI CLARK, GEOFFREY J. · 2010 to 2014
$1.3M
NCI NIH HHS R01 CA133171NCI NIH HHS T32 CA009171
6 · The paper itself

Abstract

The Ras genes are the most frequently mutated oncogenes in human cancer. However, Ras biology is quite complex. While Ras promotes tumorigenesis by regulating numerous growth promoting pathways, activated Ras can paradoxically also lead to cell cycle arrest, death, and Oncogene-Induced Senescence (OIS). OIS is thought to be a critical pathway that serves to protect cells against aberrant Ras signaling. Multiple reports have highlighted the importance of the p53 and Rb tumor suppressors in Ras mediated OIS. However, until recently, the molecular mechanisms connecting Ras to these proteins remained unknown. The RASSF family of tumor suppressors has recently been identified as direct effectors of Ras. One of these members, NORE1A (RASSF5), may be the missing link between Ras-induced senescence and the regulation of p53 and Rb. This occurs both quantitatively, by promoting protein stability, as well as qualitatively via promoting critical pro-senescent post-translational modifications. Here we review the mechanisms by which NORE1A can activate OIS as a barrier against Ras-mediated transformation, and how this could lead to improved therapeutic strategies against cancers having lost NORE1A expression.

Indexed as

Cell ProliferationCellular SenescenceGenes, Tumor SuppressorOncogenesAdaptor Proteins, Signal TransducingAnimalsApoptosis Regulatory ProteinsCell Transformation, NeoplasticGene Expression Regulation, NeoplasticGenetic Predisposition to DiseaseHumansMonomeric GTP-Binding ProteinsNeoplasmsPhenotyperas ProteinsRetinoblastoma ProteinAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsMonomeric GTP-Binding Proteinsras ProteinsRASSF5 protein, humanRetinoblastoma ProteinTP53 protein, humanTumor Suppressor Protein p53HIPK2p53PP1ARasRASSFRetinoblastoma

Identifiers

PMID28455242
PMCPMC5502528
OpenAlexW2608289720

What OpenQuestion holds

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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.