Evidence map›Paper›PMID 27535224›Full record

ArticleThe Journal of biological chemistry2016

The Breast Cancer Tumor Suppressor TRIM29 Is Expressed via ATM-dependent Signaling in Response to Hypoxia.

Muzaffer Dükel, W Scott Streitfeld, Tsz Ching Chloe Tang, Lindsey R F Backman, Lingbao Ai, W Stratford May, Kevin D Brown

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

16 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Clinical significance of TRIM29 expression in patients with gastric cancer.Gastroenterology and hepatology from bed to bench · 2022
    Article
  9. Review
  10. Article
  11. Frontiers in physiology · 2020
    Article
  12. Regulation of Gene Expression under Hypoxic Conditions.International journal of molecular sciences · 2019
    Review
  13. Article
  14. Article
  15. Article
  16. 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 1 institution in 1 country.

Muzaffer DükelFrom the Departments of Biochemistry and Molecular Biology and.
W Scott StreitfeldMedicine, University of Florida College of Medicine, Gainesville, Florida 32610.
Tsz Ching Chloe TangMedicine, University of Florida College of Medicine, Gainesville, Florida 32610.
Lindsey R F BackmanFrom the Departments of Biochemistry and Molecular Biology and.
Lingbao AiFrom the Departments of Biochemistry and Molecular Biology and.
W Stratford MayMedicine, University of Florida College of Medicine, Gainesville, Florida 32610.
Kevin D BrownFrom the Departments of Biochemistry and Molecular Biology and kdbrown1@ufl.edu.
University of Florida · US

Funding

TUMOR ANTIGENS THAT ELICIT HUMORAL IMMUNE RESPONSES IN CANCER PATIENTSP01CA012582 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MORTON, DONALD L · 1985 to 2010
$40.8M
NCI NIH HHS P01 CA012582
6 · The paper itself

Abstract

Reduced ATM function has been linked to breast cancer risk, and the TRIM29 protein is an emerging breast cancer tumor suppressor. Here we show that, in cultured breast tumor and non-tumorigenic mammary epithelial cells, TRIM29 is up-regulated in response to hypoxic stress but not DNA damage. Hypoxia-induced up-regulation of TRIM29 is dependent upon ATM and HIF1α and occurs through increased transcription of the TRIM29 gene. Basal expression of TRIM29 is also down-regulated in cells expressing diminished levels of ATM, and findings suggest that this occurs through basal NF-κB activity as knockdown of the NF-κB subunit RelA suppresses TRIM29 abundance. We have previously shown that the activity of the TWIST1 oncogene is antagonized by TRIM29 and now show that TRIM29 is necessary to block the up-regulation of TWIST1 that occurs in response to hypoxic stress. This study establishes TRIM29 as a hypoxia-induced tumor suppressor gene and provides a novel molecular mechanism for ATM-dependent breast cancer suppression.

Indexed as

Signal TransductionAtaxia Telangiectasia Mutated ProteinsBreast NeoplasmsCell HypoxiaCell Line, TumorDNA-Binding ProteinsFemaleHumansNF-kappa BNuclear ProteinsTranscription FactorsTumor Suppressor ProteinsTwist-Related Protein 1Ataxia Telangiectasia Mutated ProteinsATM protein, humanDNA-Binding ProteinsNF-kappa BNuclear ProteinsTranscription FactorsTRIM29 protein, humanTumor Suppressor ProteinsTWIST1 protein, humanTwist-Related Protein 1breast cancercell signalinghypoxiahypoxia-inducible factor (HIF)tumor suppressor gene

Identifiers

PMID27535224
PMCPMC5076825
OpenAlexW2516625751

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.