Evidence map›Paper›PMID 40877987›Full record

ArticleHereditas2025

Decoding the PTTG family's contribution to LUAD pathogenesis: a comprehensive study on expression, epigenetics, and therapeutic interventions.

Jinna Di, Li Tian, Fan Yan, Zhang Zhe, Cai Lin, Liu Jingyu

Erratum issuedAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Hereditas, 2025. 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 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

5 · Who and what money

Authors and funding

6 authors.

Jinna DiDepartment of Respiratory and Critical Care Medicine, The Third Affiliated Hospital of Jinzhou Medical University, No. 2 Section 5 Heping Road, Linghe District, Jinzhou, 121000, Liaoning, China.
Li TianDepartment of Respiratory and Critical Care Medicine, The Third Affiliated Hospital of Jinzhou Medical University, No. 2 Section 5 Heping Road, Linghe District, Jinzhou, 121000, Liaoning, China.
Fan YanDepartment of Respiratory and Critical Care Medicine, The Third Affiliated Hospital of Jinzhou Medical University, No. 2 Section 5 Heping Road, Linghe District, Jinzhou, 121000, Liaoning, China.
Zhang ZheDepartment of Respiratory and Critical Care Medicine, The Third Affiliated Hospital of Jinzhou Medical University, No. 2 Section 5 Heping Road, Linghe District, Jinzhou, 121000, Liaoning, China.
Cai LinDepartment of Respiratory and Critical Care Medicine, The Third Affiliated Hospital of Jinzhou Medical University, No. 2 Section 5 Heping Road, Linghe District, Jinzhou, 121000, Liaoning, China.
Liu JingyuDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Jinzhou Medical University, No. 2 Section 5 Guta Road, Renmin District, Jinzhou, 121000, Liaoning, China. Jinna_Di@163.com.

Funding

Liaoning Provincial Department of Science and Technology 2024-MSLH-167
6 · The paper itself

Abstract

backgroundLung adenocarcinoma (LUAD) stands as a prevalent malignancy, yet its pathology remains incompletely comprehended.

methodsIn this comprehensive study, we explored the roles of the pituitary tumor-transforming gene (PTTG) family, including PTTG1, PTTG2, and the pseudogene PTTG3P in lung adenocarcinoma (LUAD). Employing a multi-faceted approach, we conducted in-depth analyses using clinical samples and expression datasets.

resultsOur findings revealed a significant up-regulation of PTTG family genes in LUAD cell lines and tissue samples compared to adjacent normal controls, suggesting their potential as diagnostic biomarkers. Through promoter methylation and mutational analyses, we uncovered regulatory mechanisms influencing PTTG gene expression. The exploration of the PTTG family's impact on LUAD patient survival demonstrated their association with adverse outcomes, emphasizing their potential prognostic relevance. Moreover, functional assays demonstrated that the knockdown of PTTG1 and PTTG2 genes resulted in the reduction of cell proliferation, colony formation, and cell migration abilities in A549 and H1975 LUAD cells. Furthermore, our investigation extended to therapeutic avenues, where we identified Calcitriol as a potential drug within the DrugBank database to down-regulate PTTG genes. Molecular docking analyses provided insights into the strong interaction between Calcitriol and PTTG1/PTTG2 proteins, laying the groundwork for further exploration of Calcitriol in LUAD treatment.

conclusionIn conclusion, this study contributes a comprehensive understanding of the PTTG family's involvement in LUAD, shedding light on their diagnostic, prognostic, and therapeutic implications.

Indexed as

Adenocarcinoma of LungEpigenesis, GeneticLung NeoplasmsSecurinCell Line, TumorCell MovementCell ProliferationDNA MethylationGene Expression Regulation, NeoplasticHumansMolecular Docking SimulationPromoter Regions, Geneticpituitary tumor-transforming protein 1, humanSecurinBiomarkerGene expressionLUADMutationsPTTG genesTreatment

Identifiers

PMID40877987
PMCPMC12395852

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.