Evidence map›Paper›PMID 39027522›Full record

ArticleHeliyon2024

Hyper-methylation and DNMT3A mediated LTC4S downregulation promoted lung adenocarcinoma tumorigenesis via mTORC1 signaling pathway.

Yang Ren, Peng Zhang, Liqun Li, Mei Wang, Huiliang Hu, Yidan Shen, Ping Xu, Qingguo Wu, Feng Li

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

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

1 citing paper in PubMed.

  1. 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

9 authors.

Yang RenDepartment of Respiratory Disease and Critical Care Medicine, Shanghai Public Health Clinical Center, Fudan University, Shanghai, 201508, China.
Peng ZhangDepartment of Respiratory Disease and Critical Care Medicine, Shanghai Public Health Clinical Center, Fudan University, Shanghai, 201508, China.
Liqun LiDepartment of Respiratory Disease and Critical Care Medicine, Shanghai Public Health Clinical Center, Fudan University, Shanghai, 201508, China.
Mei WangDepartment of Respiratory Disease and Critical Care Medicine, Shanghai Public Health Clinical Center, Fudan University, Shanghai, 201508, China.
Huiliang HuDepartment of Respiratory Disease and Critical Care Medicine, Shanghai Public Health Clinical Center, Fudan University, Shanghai, 201508, China.
Yidan ShenDepartment of Respiratory Disease and Critical Care Medicine, Shanghai Public Health Clinical Center, Fudan University, Shanghai, 201508, China.
Ping XuDepartment of Respiratory Disease and Critical Care Medicine, Shanghai Public Health Clinical Center, Fudan University, Shanghai, 201508, China.
Qingguo WuDepartment of Respiratory Disease and Critical Care Medicine, Shanghai Public Health Clinical Center, Fudan University, Shanghai, 201508, China.
Feng LiDepartment of Respiratory Disease and Critical Care Medicine, Shanghai Public Health Clinical Center, Fudan University, Shanghai, 201508, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Lung adenocarcinoma is a malignancy characterized by high mortality rates and unfavorable prognosis. However, the role of Leukotriene C4 Synthase (LTC4S) in lung cancer remains uninvestigated. Methods: The expression and prognostic value of LTC4S in LUAD were analyzed using the GEPIA online database. Subsequently, the function of LTC4S in lung cancer cells was examined through gain-of function experiments, using assays to evaluate tumor malignant behavior. Subcutaneous xenograft experiments in vivo was used for investigating the functions of LTC4S. Then, tumor hallmark pathways were analyzed by GSEA. Western blot assay was used to validate the impact of LTC4S on mTORC1 pathway. Finally, the correlation of mRNA and methylation of LTC4S were analyzed by cBioPortal. qRT-PCR, ChIP-qPCR and ChIP-Atlas were used to verify the regulation factors of LTC4S low expression in LUAD cells. Results: LTC4S presented significant decreased expression and favorable prognostic significance in LUAD. LTC4S was correlated with clinical stages in LUAD, which showed decreased expression gradually and significantly along with TNM stages. LTC4S-co-expressed genes were closely related to Ras signaling pathway, and MAPK signaling pathway. Overexpression of LTC4S inhibited cancer malignant phenotype and tumor growth in vitro Conclusions: In conclusion, low expression of LTC4S serves as an unfavorable prognostic marker and the critical function of LTC4S in controlling the progression of LUAD. This highlights the promise for exploring the clinical benefits of manipulating LTC4S in LUAD targeted therapies.

Indexed as

DNA methylationLeukotriene C4 Synthase (LTC4S)Lung adenocarcinoma (LUAD)mTORC1 signaling pathwayPrognosis

Identifiers

PMID39027522
PMCPMC11255598

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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.