Evidence map›Paper›PMID 18172554›Full record

ArticleThe Journal of clinical investigation2008

The aryl hydrocarbon receptor repressor is a putative tumor suppressor gene in multiple human cancers.

Enrique Zudaire, Natalia Cuesta, Vundavalli Murty, Karen Woodson, Lisa Adams, Nieves Gonzalez, Alfredo Martínez, Gopeshwar Narayan, Ilan Kirsch, Wilbur Franklin and 3 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
122citing papers in PubMed, 3 pooled it
5.2field-weighted citation impact, top 4% 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

122 citing papers in PubMed, 3 syntheses or guidelines pooled it, 213 citations in OpenAlex.

  1. Pooled it
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  19. AhRR and PPP1R3C: Potential Prognostic Biomarkers for Serous Ovarian Cancer.International journal of molecular sciences · 2023
    Article
  20. Article

62 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

13 authors at 1 institution in 1 country.

Enrique ZudaireAngiogenesis Core Facility, NCI, NIH, Gaithersburg, Maryland 20892-4605, USA. zudairee@mail.nih.gov
Natalia Cuesta
Vundavalli Murty
Karen Woodson
Lisa Adams
Nieves Gonzalez
Alfredo Martínez
Gopeshwar Narayan
Ilan Kirsch
Wilbur Franklin
Fred Hirsch
Michael Birrer
Frank Cuttitta
Angiogenesis Foundation · US

Funding

Tissue Bank and Biomarkers CoreP50CA058187 · NCI · UNIVERSITY OF COLORADO DENVER · PI MILLER, YORK E · 1992 to 2018
$43.8M
Molecular Profiling of Clinical SpecimensZICBC011040 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI EDELMAN, DANIEL · 2009 to 2020
$25.5M
Trans-NIH Angiogenesis Core FacilityZICBC010964 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI CUTTITTA, FRANK · 2009 to 2010
$2.1M
USE OF TRANSCRIPTIONAL FACTORS AS TARGETS AND AGENTS IN CARCINOGENESISZ01SC000165 · SC · DIVISION OF CLINICAL SCIENCES - NCI · PI BIRRER, MICHAEL · 1996 to 2008
$974k
Molecular Profiling of Clinical SpecimensZ01BC011040 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI MELTZER, PAUL S. · 2008 to 2008
$773k
The Use of Transcriptional Factors as Targets and Agents in CarcinogenesisZIASC000165 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI BIRRER, MICHAEL · 2009 to 2009
$187k
Trans-NIH Angiogenesis Core FacilityZ01BC010964 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI CUTTITTA, FRANK · 2008 to 2008
$42k
Peptide Growth Factors That Regulate Tumor ProliferationZ01SC000173 · SC · CLINICAL SCIENCES · PI CUTTITTA, FRANK · 1996 to 2005
–
Intramural NIH HHS Z01 SC000173NCI NIH HHS 5P50 CA 058187NCI NIH HHS P50 CA058187
6 · The paper itself

Abstract

The aryl hydrocarbon receptor repressor (AHRR) is a bHLH/Per-ARNT-Sim transcription factor located in a region of chromosome 5 (5p15.3) that has been proposed to contain one or more tumor suppressor genes. We report here consistent downregulation of AHRR mRNA in human malignant tissue from different anatomical origins, including colon, breast, lung, stomach, cervix, and ovary, and demonstrate DNA hypermethylation as the regulatory mechanism of AHRR gene silencing. Knockdown of AHRR gene expression in a human lung cancer cell line using siRNA significantly enhanced in vitro anchorage-dependent and -independent cell growth as well as cell growth after transplantation into immunocompromised mice. In addition, knockdown of AHRR in non-clonable normal human mammary epithelial cells enabled them to grow in an anchorage-independent manner. Further, downregulation of AHRR expression in the human lung cancer cell line conferred resistance to apoptotic signals and enhanced motility and invasion in vitro and angiogenic potential in vivo. Ectopic expression of AHRR in tumor cells resulted in diminished anchorage-dependent and -independent cell growth and reduced angiogenic potential. These results therefore demonstrate that AHRR is a putative new tumor suppressor gene in multiple types of human cancers.

Indexed as

AnimalsApoptosisCell CycleCell Line, TumorCell MovementGenes, Tumor SuppressorHumansMiceNeoplasmsNeoplasm TransplantationReceptors, Aryl HydrocarbonRNA, Small InterferingReceptors, Aryl HydrocarbonRNA, Small Interfering

Identifiers

PMID18172554
PMCPMC2157559
OpenAlexW1980462928

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.