Evidence map›Paper›PMID 34419073›Full record

ArticleCancer cell international2021

NCAPG promotes the progression of lung adenocarcinoma via the TGF-β signaling pathway.

Yun Wu, Ying Lin, Junfan Pan, Xunwei Tu, Yiquan Xu, Hongru Li, Yusheng Chen

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
5.6field-weighted citation impact, top 3% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
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  3. In smokers, the axis NCAPG/hsa-let-7b-5p/TMPO-AS1 promotes lung adenocarcinoma.Reports of practical oncology and radiotherapy : journal of Greatpoland Cancer Center in Poznan and Polish Society of Radiation Oncology · 2025
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  7. NCPAD2 is a favorable predictor of prognostic and immunotherapeutic biomarker for multiple cancer types including lung cancer.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 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

7 authors at 1 institution in 1 country.

Yun Wu *Shengli Clinical Medical College of Fujian Medical University, Fuzhou, 350001, China.
Ying Lin *Shengli Clinical Medical College of Fujian Medical University, Fuzhou, 350001, China.
Junfan PanShengli Clinical Medical College of Fujian Medical University, Fuzhou, 350001, China.
Xunwei TuShengli Clinical Medical College of Fujian Medical University, Fuzhou, 350001, China.
Yiquan XuShengli Clinical Medical College of Fujian Medical University, Fuzhou, 350001, China.
Hongru LiShengli Clinical Medical College of Fujian Medical University, Fuzhou, 350001, China. muzi131122@163.com.
Yusheng ChenShengli Clinical Medical College of Fujian Medical University, Fuzhou, 350001, China. cysktz@fjmu.edu.cn.ORCID http://orcid.org/0000-0002-0048-0169
Fujian Medical University · CN

Funding

Health research talents training program of Fujian province 2019-ZQNB-1high-level hospital grants from Fujian Provincial Hospital, Fujian province, China 2018GSP008Natural Science Foundation of China 82002457Startup Fund for scientific research, Fujian Medical University 2018QH1130Startup Fund for scientific research, Fujian Medical University 2019QH2045
6 · The paper itself

Abstract

backgroundLung cancer has the highest case fatality rate among cancers because of uncontrolled proliferation and early metastasis of cancer cells in the lung tissue. This study aimed to clarify the role of the non-SMC condensin I complex, subunit G (NCAPG) in lung adenocarcinoma (LUAD), explore the mechanisms of its progression, and lay the foundation for the search for new biological markers.

methodsWe analyzed overlapping differentially expressed genes (DEGs) from three datasets; a protein-protein interaction (PPI) network was subsequently constructed and analyzed using Cytoscape. We then selected NCAPG for validation because of its poor prognosis and because it has not been sufficiently studied in the context of LUAD. Immunohistochemical analysis was used to detect the expression of NCAPG in LUAD tissues, and the relationships between NCAPG and clinical parameters were analyzed. In vitro and in vivo experiments were conducted to verify the role of NCAPG in LUAD. Finally, we studied the specific mechanism of action of NCAPG in LUAD.

resultsThrough comprehensive analysis of the GSE43458, GSE75037, and The Cancer Genome Atlas databases, we identified 517 overlapping DEGs. Among them, NCAPG was identified as a hub gene. Immunohistochemical analysis revealed that NCAPG was strongly associated with the clinical stage, M-classification, and N-classification. Univariate and multivariate Cox regression analyses indicated that NCAPG was a prognostic risk factor for LUAD, while the in vitro experiments showed that NCAPG overexpression promoted proliferation, migration, invasion, and epithelial-mesenchymal transition. Furthermore, knockdown of NCAPG inhibited LUAD progression, both in vitro and in vivo. Mechanistically, NCAPG overexpression increased p-Smad2 and p-Smad3 expressions in the transforming growth factor β (TGF-β) signaling pathway. Additionally, rescue experiments indicated that TGF-β signaling pathway inhibitors could restore the effect of NCAPG overexpression in LUAD cells.

conclusionsNCAPG may promote proliferation and migration via the TGF-β signaling pathway in LUAD.

Indexed as

Lung adenocarcinomaNCAPGPrognostic biomarkersTGF-β signaling pathway

Identifiers

PMID34419073
PMCPMC8380402
OpenAlexW3195306291

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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.