Evidence map›Paper›PMID 33921748›Full record

ArticleInternational journal of molecular sciences2021

ATF3 Promotes Arsenic-Induced Apoptosis and Oppositely Regulates DR5 and Bcl-xL Expression in Human Bronchial Epithelial Cells.

Qiwen Shi, Bei Hu, Chen Yang, Lan Zhao, Jing Wu, Nan Qi

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.4field-weighted citation impact, top 13% 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

14 citing papers in PubMed, 27 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Qiwen ShiCollaborative Innovation Center of Yangtze River Delta Region Green Pharmaceuticals, Institute of Engineering Biology and Health, College of Pharmaceutical Sciences, Zhejiang University of Technology, Hangzhou 310014, China.ORCID 0000-0002-8692-1374
Bei HuCollaborative Innovation Center of Yangtze River Delta Region Green Pharmaceuticals, Institute of Engineering Biology and Health, College of Pharmaceutical Sciences, Zhejiang University of Technology, Hangzhou 310014, China.
Chen YangCollaborative Innovation Center of Yangtze River Delta Region Green Pharmaceuticals, Institute of Engineering Biology and Health, College of Pharmaceutical Sciences, Zhejiang University of Technology, Hangzhou 310014, China.
Lan ZhaoCollaborative Innovation Center of Yangtze River Delta Region Green Pharmaceuticals, Institute of Engineering Biology and Health, College of Pharmaceutical Sciences, Zhejiang University of Technology, Hangzhou 310014, China.
Jing WuCollaborative Innovation Center of Yangtze River Delta Region Green Pharmaceuticals, Institute of Engineering Biology and Health, College of Pharmaceutical Sciences, Zhejiang University of Technology, Hangzhou 310014, China.
Nan QiCollaborative Innovation Center of Yangtze River Delta Region Green Pharmaceuticals, Institute of Engineering Biology and Health, College of Pharmaceutical Sciences, Zhejiang University of Technology, Hangzhou 310014, China.ORCID 0000-0002-1423-7709
Zhejiang University of Technology · CN

Funding

National Natural Science Foundation of China 31870864National Natural Science Foundation of China 81703181Natural Science Foundation of Zhejiang Province LY20C080003
6 · The paper itself

Abstract

Arsenic is one of the most common environmental pollutants eliciting serious public health issues; however, it is also a well-recognized chemotherapeutic agent for acute promyelocytic leukemia. The association between arsenic exposure and lung diseases has been established, but underlying molecular mechanisms are poorly defined. Here we investigated the toxicology of arsenic in airway epithelium. Arsenic rapidly induced the activating transcription factor ATF3 expression through the JNK and p38 pathways. The ATF3-deficient BEAS-2B cells were relatively resistant to apoptosis upon arsenic exposure, indicating a facilitatory role of ATF3 in arsenic-induced apoptosis. We further showed that ATF3 oppositely regulated the transcription of death receptor (DR5) and Bcl2-like 1 (Bcl-xL) by directly binding to the promoter DR5 and Bcl-xL. Altogether, our findings establish ATF3 as a pro-apoptotic protein in arsenic-induced airway epithelial apoptosis through transcriptionally regulating DR5 and Bcl-xL, highlighting the potential of ATF3 as an early and sensitive biomarker for arsenic-caused lung injury.

Indexed as

Activating Transcription Factor 3ApoptosisArsenicBronchiCell Line, TumorEpithelial CellsHumansMAP Kinase Signaling SystemPromoter Regions, GeneticReceptors, TNF-Related Apoptosis-Inducing LigandActivating Transcription Factor 3ArsenicReceptors, TNF-Related Apoptosis-Inducing LigandTNFRSF10B protein, humanapoptosisarsenicATF3Bcl-xLDR5

Identifiers

PMID33921748
PMCPMC8072958
OpenAlexW3153341272

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.