Evidence map›Paper›PMID 26909609›Full record

ArticleOncotarget2016

Aryl hydrocarbon receptor nuclear translocator (ARNT) isoforms control lymphoid cancer cell proliferation through differentially regulating tumor suppressor p53 activity.

Kacie A Gardella, Israel Muro, Gloria Fang, Krishnakali Sarkar, Omayra Mendez, Casey W Wright

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

19 citing papers in PubMed, 24 citations in OpenAlex.

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  9. AhR promotes phosphorylation of ARNT isoform 1 in human T cell malignancies as a switch for optimal AhR activity.Proceedings of the National Academy of Sciences of the United States of America · 2022
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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

6 authors at 1 institution in 1 country.

Kacie A GardellaInstitute for Cellular and Molecular Biology, The University of Texas at Austin, Austin, TX, USA.
Israel MuroDivision of Pharmacology and Toxicology, and The Center for Molecular and Cellular Toxicology, College of Pharmacy, The University of Texas at Austin, Austin, TX, USA.
Gloria FangDivision of Pharmacology and Toxicology, and The Center for Molecular and Cellular Toxicology, College of Pharmacy, The University of Texas at Austin, Austin, TX, USA.
Krishnakali SarkarInstitute for Cellular and Molecular Biology, The University of Texas at Austin, Austin, TX, USA.
Omayra MendezInstitute for Cellular and Molecular Biology, The University of Texas at Austin, Austin, TX, USA.
Casey W WrightDivision of Pharmacology and Toxicology, and The Center for Molecular and Cellular Toxicology, College of Pharmacy, The University of Texas at Austin, Austin, TX, USA.
The University of Texas at Austin · US

Funding

Training in Molecular Toxicology/Environmental DiseaseT32ES007247 · NIEHS · UNIVERSITY OF TEXAS AUSTIN · PI RICHBURG, JOHN H · 1990 to 2014
$2.9M
Novel ARNT-mediated Regulatory Paradigm of AHR SignalingR01ES025809 · NIEHS · UNIVERSITY OF TEXAS MED BR GALVESTON · PI WRIGHT, CASEY W · 2016 to 2021
$1.9M
NIEHS NIH HHS R01 ES025809NIEHS NIH HHS T32 ES007247
6 · The paper itself

Abstract

The aryl hydrocarbon receptor nuclear translocator (ARNT) is involved in xenobiotic and hypoxic responses, and we previously showed that ARNT also regulates nuclear factor-κB (NF-κB) signaling by altering the DNA binding activity of the RelB subunit. However, our initial study of ARNT-mediated RelB modulation was based on simultaneous suppression of the two ARNT isoforms, isoform 1 and 3, and precluded the examination of their individual functions. We find here that while normal lymphocytes harbor equal levels of isoform 1 and 3, lymphoid malignancies exhibit a shift to higher levels of ARNT isoform 1. These elevated levels of ARNT isoform 1 are critical to the proliferation of these cancerous cells, as suppression of isoform 1 in a human multiple myeloma (MM) cell line, and an anaplastic large cell lymphoma (ALCL) cell line, triggered S-phase cell cycle arrest, spontaneous apoptosis, and sensitized cells to doxorubicin treatment. Furthermore, co-suppression of RelB or p53 with ARNT isoform 1 prevented cell cycle arrest and blocked doxorubicin induced apoptosis. Together our findings reveal that certain blood cancers rely on ARNT isoform 1 to potentiate proliferation by antagonizing RelB and p53-dependent cell cycle arrest and apoptosis. Significantly, our results identify ARNT isoform 1 as a potential target for anticancer therapies.

Indexed as

Alternative SplicingAryl Hydrocarbon Receptor Nuclear TranslocatorCell DifferentiationCell Line, TumorCell ProliferationDoxorubicinHumansJurkat CellsLymphomaProtein IsoformsSignal TransductionTumor Suppressor Protein p53ARNT protein, humanAryl Hydrocarbon Receptor Nuclear TranslocatorDoxorubicinProtein IsoformsTP53 protein, humanTumor Suppressor Protein p53alternative splicingARNTlymphoid malignanciesp53RelB

Identifiers

PMID26909609
PMCPMC4905433
OpenAlexW2288322784

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.