Evidence map›Paper›PMID 37254219›Full record

ArticleHereditas2023

NPM3 as a novel oncogenic factor and poor prognostic marker contributes to cell proliferation and migration in lung adenocarcinoma.

Shan Wei, Jing Xing, Kaining Lu, Kai Wang, Wanjun Yu

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

Article in Hereditas, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
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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

5 authors at 4 institutions in 1 country.

Shan WeiDepartment of Respiratory and Critical Care Medicine, The Fourth Affiliated Hospital, School of Medicine, Zhejiang University, Yiwu, 322000, Zhejiang, People's Republic of China.
Jing XingDepartment of Respiratory and Critical Care Medicine, The Affiliated People's Hospital of Ningbo University (Ningbo Yinzhou People's Hospital), No.251, Baizhang Road, Ningbo, 315040, Zhejiang, People's Republic of China.
Kaining LuDepartment of Urology, The Affiliated First Hospital of Ningbo University (Ningbo First Hospital), No.59, Liuting Street, Ningbo, 315010, Zhejiang, People's Republic of China.
Kai WangDepartment of Respiratory and Critical Care Medicine, The Fourth Affiliated Hospital, School of Medicine, Zhejiang University, Yiwu, 322000, Zhejiang, People's Republic of China.
Wanjun YuDepartment of Respiratory and Critical Care Medicine, The Affiliated People's Hospital of Ningbo University (Ningbo Yinzhou People's Hospital), No.251, Baizhang Road, Ningbo, 315040, Zhejiang, People's Republic of China. nbyuwanjun@163.com.
Ningbo University · CNNingbo No.6 Hospital · CNNingbo University of Technology · CNZhejiang University · CN

Funding

Medical Science and Technology Project of Zhejiang Province 2023KY303Project of NINGBO Leading Medical & Health Discipline 2022-B19
6 · The paper itself

Abstract

backgroundLung cancer is the leading cause of cancer-related deaths worldwide, and despite recent advances in targeted therapies and immunotherapies, the clinical benefit remains limited. Therefore, there is an urgent need to further investigate the molecular mechanisms underlying lung cancer. The aim of this study was to investigate the expression and function of NPM3 in the tumor microenvironment of lung adenocarcinoma (LUAD).

methodsWe utilized bioinformatics tools and databases, including UALCAN, GEPIA2, HPA, and Sangerbox, to analyze NPM3 expression in LUAD samples and its association with prognosis and mutational landscape. NPM3 expression in various cell types was assessed at the single cell level using the TISCH database. We also used algorithms such as TIMER and EPIC to explore the crosstalk between NPM3 expression and immune features. KEGG enrichment analysis was performed to identify potential signaling pathways of NPM3. Finally, we employed siRNA knockdown strategy to investigate the effect of NPM3 on LUAD cell proliferation and migration in vitro.

resultsNPM3 was significantly upregulated in LUAD tissues and was strongly associated with poor prognosis and TP53 gene mutations. Single-cell sequencing analysis revealed that NPM3 was expressed in immune cells (dendritic cells and monocytes/macrophages) in the tumor microenvironment. Moreover, NPM3 expression was negatively associated with immune B cell and CD4 T cell infiltration, as well as with several immune-related genes (including CCL22, CXCR2, CX3CR1, CCR6, HLA-DOA, HLA-DQA2). KEGG enrichment analysis indicated that NPM3 expression was associated with cell cycle, CAMs, and NSCLC pathway genes. Finally, in vitro experiments showed that NPM3 knockdown inhibited LUAD cell proliferation and migration in NCI-H1299 and SPC-A1 cells, and suppressed the expression of CCNA2 and MAD2L1.

conclusionElevated NPM3 expression predicts poor clinical outcome and an immunosuppressive microenvironment in LUAD tissues. NPM3 promotes LUAD progression by promoting cell proliferation and migration, and targeting NPM3 may represent a novel therapeutic strategy for LUAD.

Indexed as

Adenocarcinoma of LungLung NeoplasmsNucleoplasminsCell DivisionCell ProliferationHumansPrognosisTumor MicroenvironmentNPM3 protein, humanNucleoplasminsCell migrationCell proliferationImmune microenvironmentLung adenocarcinomaNPM3Prognosis

Identifiers

PMID37254219
PMCPMC10230701
OpenAlexW4378782725

What OpenQuestion holds

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LicenceCC BY
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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.