Evidence map›Paper›PMID 32850324›Full record

ArticleFrontiers in oncology2020

Methylation-Induced Silencing of ALDH2 Facilitates Lung Adenocarcinoma Bone Metastasis by Activating the MAPK Pathway.

Mengdi Yang, AiTing Wang, Changcan Li, Jing Sun, Gang Yi, Hao Cheng, Xueni Liu, Zhiyu Wang, Yiyi Zhou, Guangyu Yao and 5 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.7field-weighted citation impact, top 8% 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

18 citing papers in PubMed, 32 citations in OpenAlex.

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  5. Prognostic Significance ofPhenomics (Cham, Switzerland) · 2024
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  7. ALDH2 activation attenuates oxygen-glucose deprivation/reoxygenation-induced cell apoptosis, pyroptosis, ferroptosis and autophagy.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
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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

15 authors at 3 institutions in 1 country.

Mengdi YangDepartment of Internal Oncology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
AiTing WangShanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Changcan LiShanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jing SunDepartment of Internal Oncology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Gang YiShanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Hao ChengShanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xueni LiuShanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Zhiyu WangDepartment of Internal Oncology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Yiyi ZhouDepartment of Internal Oncology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Guangyu YaoDepartment of Internal Oncology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Shuai WangDepartment of Internal Oncology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Rui LiangShanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Bin LiShanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Dan LiShanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Hui ZhaoDepartment of Internal Oncology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Shanghai Jiao Tong University · CNShanghai Sixth People's Hospital · CNTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bone metastasis (BM) dramatically reduces the quality of life and life expectancy in lung adenocarcinoma (LUAD) patients. There is an urgent need to identify potential biomarkers for application in the treatment of this deadly disease. We compared patient BM, LUAD, and para-LUAD tissues using proteomic analysis and identified aldehyde dehydrogenase 2 (ALDH2), which can detoxify acetaldehyde to acetic acid, as one of the key regulators in lung tumor metastasis. Both the mRNA and protein levels of ALDH2 were significantly lower in tumor tissues than in normal tissues and were lowest in BM tissues with increased migratory capacity. Also, ALDH2 was upregulated following treatment with 5-azacitidine, a DNA methyltransferase inhibitor, in H1299, H460, and HCC827 cells. Further, we identified a potential methylated CpG island 3, with the longest methylated CpG island area in ALDH2, and performed bisulfite genomic sequencing of these sites. An average of 78.18% of the sites may be methylated in CpG island 3. Knockdown of DNA (cytosine-5)-methyltransferase 3A (DNMT3A) and methylated CpG binding protein 4 (MBD4) upregulated ALDH2 expression. ALDH2 functions as a mitogen-activated protein kinase (MAPK) upstream to inhibit cell proliferation and migration, promote cell apoptosis, and alter the epithelial-mesenchymal transition (EMT) by elevating E-cadherin and attenuating vimentin. Cell proliferation and migration were inhibited after the addition of the JNK inhibitor SP600125. In the multivariate analysis, M stage (

Indexed as

ALDH2bone metastasisDNA methylationlung adenocarcinomaMAPK

Identifiers

PMID32850324
PMCPMC7406638
OpenAlexW3045541175

What OpenQuestion holds

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LicenceCC BY
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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.