Evidence map›Paper›PMID 26852918›Full record

ArticleScientific reports2016

Aryl Hydrocarbon Receptor Activates NDRG1 Transcription under Hypoxia in Breast Cancer Cells.

En-Yu Li, Wei-Yung Huang, Ya-Chu Chang, Mong-Hsun Tsai, Eric Y Chuang, Qian-Yu Kuok, Shih-Ting Bai, Lo-Yun Chao, Yuh-Pyng Sher, Liang-Chuan Lai

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In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

18 citing papers in PubMed, 26 citations in OpenAlex.

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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

10 authors at 3 institutions in 1 country.

En-Yu LiGraduate Institute of Physiology, National Taiwan University, Taipei, Taiwan.
Wei-Yung HuangGraduate Institute of Physiology, National Taiwan University, Taipei, Taiwan.
Ya-Chu ChangGraduate Institute of Physiology, National Taiwan University, Taipei, Taiwan.
Mong-Hsun TsaiInstitute of Biotechnology, National Taiwan University, Taipei, Taiwan.
Eric Y ChuangBioinformatics and Biostatistics Core, Center of Genomic Medicine, National Taiwan University, Taipei, Taiwan.
Qian-Yu KuokGraduate Institute of Clinical Medical Science, China Medical University, Taichung, Taiwan.
Shih-Ting BaiGraduate Institute of Clinical Medical Science, China Medical University, Taichung, Taiwan.
Lo-Yun ChaoGraduate Institute of Physiology, National Taiwan University, Taipei, Taiwan.
Yuh-Pyng SherGraduate Institute of Clinical Medical Science, China Medical University, Taichung, Taiwan.
Liang-Chuan LaiGraduate Institute of Physiology, National Taiwan University, Taipei, Taiwan.
National Taiwan University · TWChina Medical University · TWNational Yang Ming Chiao Tung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxia has been intensively investigated over the past several decades based on the observations that hypoxic tumors are more resistant to therapy and have a worse prognosis. Previously, we reported that N-myc downstream-regulated gene 1 (NDRG1) is strongly up-regulated under hypoxia and may play an important role in tumor adaptation to fluctuating oxygen concentrations. However, the regulatory mechanism of NDRG1 under hypoxia remains elusive. Therefore, the purpose of this study was to identify the transcription factors that regulate NDRG1 and to investigate the functional roles of NDRG1 in hypoxia. We showed that binding sites of aryl hydrocarbon receptor (AHR) were predicted in the NDRG1 promoter. Nuclear AHR was up-regulated in the presence of cobalt and hypoxia. AHR translocated to nuclei and bound between base pairs -412 and -388 of the NDRG1 promoter in hypoxia. Moreover, hypoxia-mimetic induction of NDRG1 was attenuated by knockdown of AHR expression. Also, overexpression of AHR facilitated cell proliferation and migration via up-regulation of NDRG1. These results showed for the first time that AHR positively regulates NDRG1 transcription through an AHR binding site by way of hypoxia-mimetic signaling, which may lead to development of a specific therapeutic regimen to prevent tumor malignancy under hypoxia.

Indexed as

Gene Expression RegulationHypoxiaTranscription, GeneticBinding SitesBreast NeoplasmsCell Cycle ProteinsCell Line, TumorCell ProliferationHumansIntracellular Signaling Peptides and ProteinsN-myc Downstream-Regulated Gene 1 ProteinPromoter Regions, GeneticReceptors, Aryl HydrocarbonCell Cycle ProteinsIntracellular Signaling Peptides and ProteinsN-myc Downstream-Regulated Gene 1 ProteinReceptors, Aryl Hydrocarbon

Identifiers

PMID26852918
PMCPMC4745107
OpenAlexW2414592588

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Registered trials

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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.