Evidence map›Paper›PMID 37667220›Full record

ArticleBMC cancer2023

TET2 inhibits the proliferation and metastasis of lung adenocarcinoma cells via activation of the cGAS-STING signalling pathway.

Gui Cheng, Jun Wu, Mei Ji, Wenwei Hu, Changping Wu, Jingting Jiang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC cancer, 2023. 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
3.7field-weighted citation impact, top 6% 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, 25 citations in OpenAlex.

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  17. The role of TET2 in solid tumors and its therapeutic potential: a comprehensive review.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024
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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.

Gui ChengDepartment of Tumor Biological Treatment, The Third Affiliated Hospital, Soochow University, 185 Juqian Street, Changzhou, 213003, P.R. China.
Jun WuDepartment of Tumor Biological Treatment, The Third Affiliated Hospital, Soochow University, 185 Juqian Street, Changzhou, 213003, P.R. China.
Mei JiDepartment of Tumor Biological Treatment, The Third Affiliated Hospital, Soochow University, 185 Juqian Street, Changzhou, 213003, P.R. China.
Wenwei HuDepartment of Tumor Biological Treatment, The Third Affiliated Hospital, Soochow University, 185 Juqian Street, Changzhou, 213003, P.R. China.
Changping WuDepartment of Tumor Biological Treatment, The Third Affiliated Hospital, Soochow University, 185 Juqian Street, Changzhou, 213003, P.R. China. wcpjjtt@163.com.
Jingting JiangDepartment of Tumor Biological Treatment, The Third Affiliated Hospital, Soochow University, 185 Juqian Street, Changzhou, 213003, P.R. China. jiangjingting@suda.edu.cn.
Soochow University · CN

Funding

National Natural Science Foundation of China 82072561Youth Talent Science and Technology Project of Changzhou Health Commission QN202201
6 · The paper itself

Abstract

backgroundEffective identification and development of new molecular methods for the diagnosis, treatment and prognosis of lung adenocarcinoma (LUAD) remains an urgent clinical need. DNA methylation patterns at cytosine bases in the genome are closely related to gene expression, and abnormal DNA methylation is frequently observed in various cancers. The ten-eleven translocation (TET) enzymes oxidize 5-methylcytosine (5mC) and promote locus-specific DNA methylation reversal. This study aimed to explore the role of the TET2 protein and its downstream effector, 5-hmC/5-mC DNA modification, in LUAD progression.

methodsThe expression of TET2 was analysed by real-time PCR, Western blotting and immunohistochemistry. The 5-hmC DNA content was determined by a colorimetric kit. Activation of the cGAS-STING signalling pathway was evaluated by Western blotting. CCK-8, wound healing and Transwell assays were performed to evaluate the effect of TET2 on cell proliferation, migration and invasion abilities. A xenograft model was used to analyse the effect of TET2 on the tumorigenic ability of A549 cells.

resultsTET2 overexpression decreased proliferation and metastasis of A549 and H1975 cells in vitro and in vivo. However, TET2 knockdown dramatically enhanced the proliferation, migration and invasion of A549 and H1975 cells. Mechanistically, activation of the cGAS-STING signalling pathway is critical for the TET2-mediated suppression of LUAD cell tumorigenesis and metastasis.

conclusionIn this study, we demonstrate a tumour suppressor role of TET2 in LUAD, providing new potential molecular therapeutic targets and clinical therapies for patients with non-small cell lung cancer.

Indexed as

Adenocarcinoma of LungCarcinoma, Non-Small-Cell LungDioxygenasesDNA-Binding ProteinsLung NeoplasmsCarcinogenesisCell ProliferationCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDNAHumansNucleotidyltransferasescGAS protein, humanCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDioxygenasesDNADNA-Binding ProteinsNucleotidyltransferasesTET2 protein, human5hmCcGAS-STING signalingDNA hydroxymethylationNon-Small Cell Lung CancerTET2

Identifiers

PMID37667220
PMCPMC10478367
OpenAlexW4386416720

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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.