Evidence map›Paper›PMID 40790761›Full record

ArticleEpigenetics & chromatin2025

TET1 functions as a tumor suppressor in lung adenocarcinoma through epigenetic remodeling and immune modulation.

Abdur Rahim, Brian L Ruis, Andrew T Rajczewski, Monica E Kruk, Natalia Y Tretyakova

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Epigenetics & chromatin, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

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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

4 citing papers in PubMed.

  1. Review
  2. Review
  3. Anticancer Activity ofBiomolecules · 2025
    Article
  4. 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

5 authors.

Abdur RahimDepartment of Medicinal Chemistry, College of Pharmacy, and the Epigenetic Consortium, University of Minnesota, Minneapolis, MN, 55455, USA.
Brian L RuisGenome Engineering Shared Resource, Masonic Cancer Center, University of Minnesota, Minneapolis, MN, 55455, USA.
Andrew T RajczewskiDepartment of Biochemistry, Biophysics and Molecular Biology, University of Minnesota, Minneapolis, MN, 55455, USA.
Monica E KrukDepartment of Medicinal Chemistry, College of Pharmacy, and the Epigenetic Consortium, University of Minnesota, Minneapolis, MN, 55455, USA.
Natalia Y TretyakovaDepartment of Medicinal Chemistry, College of Pharmacy, and the Epigenetic Consortium, University of Minnesota, Minneapolis, MN, 55455, USA. trety001@umn.edu.

Funding

Smoking-Induced Epigenetic Changes in the Lung: Role of DNA DemethylationR01CA095039 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI TRETYAKOVA, NATALIA Y · 2003 to 2022
$3.6M
NCI NIH HHS R01 CA095039NIH HHS R01 CA095039
6 · The paper itself

Abstract

backgroundTen-Eleven Translocation (TET1-3) dioxygenases oxidize 5-methylcytosine (5mC) in DNA to generate 5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5fC), and 5-carboxylcytosine (5caC), initiating DNA demethylation. Since their discovery in 2009, there have been contradictory reports regarding the roles of TET proteins in cancer. TET genes have been characterized as tumor suppressors because their expression levels are reduced in many human cancers including lymphoma, prostate, and pancreas, and TET2 gene mutations are common in hematological cancers. In contrast, TET1 was recently reported to be overexpressed in triple negative breast cancer and to act as a protooncogene in lung cancer.

resultsIn the present study, we employed genetic approaches to directly address the function of TET1 protein in lung adenocarcinoma. We found that overexpression (OE) of TET1 in human lung adenocarcinoma (H441, H1975) cells decreased their proliferation and inhibited colony formation, cell migration, and 3D spheroid tumorigenesis. In contrast, TET1 knockout (KO) accelerated lung adenocarcinoma cell growth and promoted colony formation, cell migration, and 3D spheroid tumorigenesis. Transcriptomics and proteomics analyses revealed that TET1 overexpression was associated with increased prevalence of immune markers, primarily via activation of the TNF and NF-kB signaling pathways. Conversely, TET1 knockout in lung adenocarcinoma cells induced the expression of genes involved in cellular metabolism and cell growth.

conclusionsOur results are consistent with tumor suppressor role of TET1 gene in lung adenocarcinoma cells (H441, H1975) and reveal its possible role in activating antitumor immunity.

Indexed as

Adenocarcinoma of LungEpigenesis, GeneticLung NeoplasmsMixed Function OxygenasesProto-Oncogene ProteinsAnimalsCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticGenes, Tumor SuppressorHumansMixed Function OxygenasesProto-Oncogene ProteinsTET1 protein, human3D spheroidDNA methylationLung cancerTET1 proteinTumor suppressor gene

Identifiers

PMID40790761
PMCPMC12337569

What Socratic holds

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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 Socratic graph.