Evidence map›Paper›PMID 35105868›Full record

ArticleNature communications2022

ΔNp63 regulates a common landscape of enhancer associated genes in non-small cell lung cancer.

Marco Napoli, Sarah J Wu, Bethanie L Gore, Hussein A Abbas, Kyubum Lee, Rahul Checker, Shilpa Dhar, Kimal Rajapakshe, Aik Choon Tan, Min Gyu Lee and 2 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. 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
2.1field-weighted citation impact, top 11% 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, 21 citations in OpenAlex.

  1. Article
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  3. DAPL1 is activated by Np63 and GRα and regulates lipid metabolism.Journal of molecular medicine (Berlin, Germany) · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 3 institutions in 1 country.

Marco Napoli *Department of Molecular Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.ORCID http://orcid.org/0000-0001-7192-5252
Sarah J Wu *Department of Molecular Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.
Bethanie L GoreDepartment of Molecular Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.
Hussein A AbbasDepartment of Molecular Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.ORCID http://orcid.org/0000-0003-2946-3562
Kyubum LeeDepartment of Biostatistics and Bioinformatics, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.
Rahul CheckerDepartment of Molecular Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.
Shilpa DharDepartment of Molecular and Cellular Oncology, University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Kimal RajapaksheDepartment of Molecular and Cell Biology, Baylor College of Medicine, Houston, TX, USA.
Aik Choon TanDepartment of Biostatistics and Bioinformatics, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.
Min Gyu LeeDepartment of Molecular and Cellular Oncology, University of Texas MD Anderson Cancer Center, Houston, TX, USA. mglee@mdanderson.org.
Cristian CoarfaDepartment of Molecular and Cell Biology, Baylor College of Medicine, Houston, TX, USA. coarfa@bcm.edu.ORCID http://orcid.org/0000-0002-4183-4939
Elsa R FloresDepartment of Molecular Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA. elsa.flores@moffitt.org.ORCID http://orcid.org/0000-0002-6173-2403
Moffitt Cancer Center · USBaylor College of Medicine · USThe University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI DAVID R ROWLEY · 2007 to 2026
$73.9M
Project 5: Pyolytic conversion of PAHs in contaminated sediments into char to eliminate toxicity and enhance soil fertilityP42ES027725 · NIEHS · BAYLOR COLLEGE OF MEDICINE · PI BHAGAVATULA MOORTHY · 2020 to 2026
$17.8M
Translational Research Support CoreP30ES030285 · NIEHS · BAYLOR COLLEGE OF MEDICINE · PI Cheryl L. Walker · 2019 to 2026
$14.7M
Identification of non-coding RNAs to therapeutically target undruggable pathways in metastatic lung adenocarcinoma and squamous cell carcinomaR35CA197452 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI FLORES, ELSA R · 2016 to 2022
$6.4M
TRAINING PROGRAM IN MOLECULAR GENETICS OF CANCERT32CA009299 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LOZANO, GUILLERMINA · 1985 to 2014
$4.7M
Role of the Histone Methyltransferase MLL4 in MedulloblastomaR01CA207109 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LEE, MIN GYU · 2017 to 2021
$1.9M
Role of the Histone Modifier KDM2A in Lung CancerR01CA207098 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LEE, MIN GYU · 2017 to 2021
$1.8M
Integrated Program in Cancer and Data Science (ICADS)T32CA233399 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI William Douglas Cress, Elsa R Flores · 2019 to 2026
$1.7M
NCI NIH HHS P30 CA016672NCI NIH HHS P30 CA125123NCI NIH HHS R01 CA207098NCI NIH HHS R01 CA207109NCI NIH HHS R35 CA197452NCI NIH HHS T32 CA009299NCI NIH HHS T32 CA233399NIEHS NIH HHS P30 ES030285NIEHS NIH HHS P42 ES027725
6 · The paper itself

Abstract

Distinct lung stem cells give rise to lung adenocarcinoma (LUAD) and squamous cell carcinoma (LUSC). ΔNp63, the p53 family member and p63 isoform, guides the maturation of these stem cells through the regulation of their self-renewal and terminal differentiation; however, the underlying mechanistic role regulated by ∆Np63 in lung cancer development has remained elusive. By utilizing a ΔNp63-specific conditional knockout mouse model and xenograft models of LUAD and LUSC, we found that ∆Np63 promotes non-small cell lung cancer by maintaining the lung stem cells necessary for lung cancer cell initiation and progression in quiescence. ChIP-seq analysis of lung basal cells, alveolar type 2 (AT2) cells, and LUAD reveals robust ∆Np63 regulation of a common landscape of enhancers of cell identity genes. Importantly, one of these genes, BCL9L, is among the enhancer associated genes regulated by ∆Np63 in Kras-driven LUAD and mediates the oncogenic effects of ∆Np63 in both LUAD and LUSC. Accordingly, high BCL9L levels correlate with poor prognosis in LUAD patients. Taken together, our findings provide a unifying oncogenic role for ∆Np63 in both LUAD and LUSC through the regulation of a common landscape of enhancer associated genes.

Indexed as

Gene Expression Regulation, NeoplasticAdenocarcinoma of LungAnimalsCarcinoma, Non-Small-Cell LungCarcinoma, Squamous CellCell Line, TumorCell ProliferationEpitheliumFemaleHumansLungLung NeoplasmsMaleMiceMice, Knockout

Identifiers

PMID35105868
PMCPMC8807845
OpenAlexW4210575033

What OpenQuestion holds

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LicenceCC BY
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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.