Evidence map›Paper›PMID 40303305›Full record

ArticleInternational journal of biological sciences2025

Aryl Hydrocarbon Receptor (AHR) Suppresses Arsenic (As

Wenxuan Zhang, Ziwei Wang, Yao Fu, Chitra Thakur, Haoyan Ji, Zhuoyue Bi, Yiran Qiu, Millie Elangbam, John Haley, Fei Chen

Abstract read
In one paragraph

Article in International journal of biological sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. 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

10 authors.

Wenxuan ZhangStony Brook Cancer Center, Department of Pathology, Renaissance School of Medicine, Stony Brook University. Lauterbur Drive, Stony Brook, NY 11794, USA.
Ziwei WangStony Brook Cancer Center, Department of Pathology, Renaissance School of Medicine, Stony Brook University. Lauterbur Drive, Stony Brook, NY 11794, USA.
Yao FuStony Brook Cancer Center, Department of Pathology, Renaissance School of Medicine, Stony Brook University. Lauterbur Drive, Stony Brook, NY 11794, USA.
Chitra ThakurStony Brook Cancer Center, Department of Pathology, Renaissance School of Medicine, Stony Brook University. Lauterbur Drive, Stony Brook, NY 11794, USA.
Haoyan JiStony Brook Cancer Center, Department of Pathology, Renaissance School of Medicine, Stony Brook University. Lauterbur Drive, Stony Brook, NY 11794, USA.
Zhuoyue BiStony Brook Cancer Center, Department of Pathology, Renaissance School of Medicine, Stony Brook University. Lauterbur Drive, Stony Brook, NY 11794, USA.
Yiran QiuStony Brook Cancer Center, Department of Pathology, Renaissance School of Medicine, Stony Brook University. Lauterbur Drive, Stony Brook, NY 11794, USA.
Millie ElangbamStony Brook Cancer Center, Department of Pathology, Renaissance School of Medicine, Stony Brook University. Lauterbur Drive, Stony Brook, NY 11794, USA.
John HaleyStony Brook Cancer Center, Department of Pathology, Renaissance School of Medicine, Stony Brook University. Lauterbur Drive, Stony Brook, NY 11794, USA.
Fei ChenStony Brook Cancer Center, Department of Pathology, Renaissance School of Medicine, Stony Brook University. Lauterbur Drive, Stony Brook, NY 11794, USA.

Funding

Reduced Reactive Oxygen Species and Oxidative Phosphorylation in Arsenic-Induced Cancer Stem CellsR01ES028263 · NIEHS · WAYNE STATE UNIVERSITY · PI CHEN, FEI · 2017 to 2021
$1.9M
Dissecting Nrf2-dependent HIF1a activation mechanism in arsenic-induced cancer stem-like cellsR01ES031822 · NIEHS · WAYNE STATE UNIVERSITY · PI CHEN, FEI · 2021 to 2025
$1.8M
Arsenic-Induced miRNA-199 and mriRNA-214 Deplete Mitochondrial DNA for the Generation of Cancer Stem-Like CellsR01ES028335 · NIEHS · WAYNE STATE UNIVERSITY · PI CHEN, FEI · 2018 to 2022
$1.3M
NIEHS NIH HHS R01 ES028263NIEHS NIH HHS R01 ES028335NIEHS NIH HHS R01 ES031822
6 · The paper itself

Abstract

Environmental arsenic (As³⁺) exposure poses a significant public health concern due to its carcinogenic potential. Our previous research suggests that As³⁺-induced carcinogenesis is mediated by inhibition of the aryl hydrocarbon receptor (AHR). However, the precise role of AHR in As³⁺-induced malignant transformation as well as cancer stem-like cell (CSC) formation, along with its underlying mechanisms, remains unclear. In this study, we used BEAS-2B cells with CRISPR-Cas9 gene editing, RNA sequencing, and immunoprecipitation to examine AHR's role in As³⁺-induced CSC development. Our findings reveal that AHR suppresses CSC formation triggered by low-dose As³⁺ (0.5 μM) via transcriptional repression of TOX, a high mobility group box DNA binding protein that play a critical role in T cell exhaustion within tumor immunology.

Indexed as

ArsenicCell Transformation, NeoplasticHigh Mobility Group ProteinsReceptors, Aryl HydrocarbonCell LineHumansNeoplastic Stem CellsArsenicHigh Mobility Group ProteinsReceptors, Aryl HydrocarbonTOX protein, humanAHRArsenicCancer stem-like cellsCarcinogenesisTOX

Identifiers

PMID40303305
PMCPMC12035900

What OpenQuestion holds

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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.