Evidence map›Paper›PMID 42311261›Full record

ArticleFrontiers in oncology2026

TPX2-mediated autophagy maintains cancer stemness in LUAD: bioinformatic screening and functional validation.

Mingzheng Jiang, Hongli Ye, Jiwei Li, Jing Wu, Xiaoyi Hu, Qiuyue Long, Liang Bu, Zhancheng Gao, Yali Zheng

Abstract read
In one paragraph

Article in Frontiers in oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Mingzheng JiangDepartment of Respiratory, Critical Care and Sleep Medicine, Xiang' an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, China.
Hongli YeDepartment of Respiratory, Critical Care and Sleep Medicine, Xiang' an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, China.
Jiwei LiDepartment of Thoracic Surgery and Oncology, the First Affiliated Hospital of Guangzhou Medical University, State Key Laboratory of Respiratory Disease & National Clinical Research Center for Respiratory Disease, Guangzhou, China.
Jing WuDepartment of Respiratory, Critical Care and Sleep Medicine, Xiang' an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, China.
Xiaoyi HuInstitute of Chest and Lung Diseases, Xiamen University, Xiamen, China.
Qiuyue LongDepartment of Respiratory, Critical Care and Sleep Medicine, Xiang' an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, China.
Liang BuInstitute of Chest and Lung Diseases, Xiamen University, Xiamen, China.
Zhancheng GaoDepartment of Respiratory, Critical Care and Sleep Medicine, Xiang' an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, China.
Yali ZhengDepartment of Respiratory, Critical Care and Sleep Medicine, Xiang' an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Targeting protein for Xklp2 (TPX2) is a known mitotic regulator overexpressed in lung adenocarcinoma (LUAD), yet its role in cancer stemness and autophagy remains unclear. Through integrative bioinformatic analysis of TCGA and GTEx datasets, we discovered that TPX2 overexpression in LUAD correlates not only with poorer overall, disease-free, disease-specific, and progression-free survival but also significantly associates with elevated stemness scores (RNAss/DNAss) and increased expression of CSC markers SOX2 and c-MYC. Functionally, CRISPR-Cas9-mediated TPX2 knockout in PC9 and H1975 cells led to marked reductions in sphere-forming capability and CSC marker expression, while TPX2 overexpression had the opposite effect. Mechanistic exploration through Co-immunoprecipitation coupled with mass spectrometry (IP-MS) and transcriptome analysis revealed a correlation between TPX2 and autophagy regulation in LUAD cells. TPX2 knockdown inhibited autophagic flux, as evidenced by decreased Beclin-1 and accumulation of p62 and LC3-II levels, together with increased GFP+/mRFP+ (yellow) LC3 puncta. Conversely, TPX2 overexpression enhanced autolysosome formation. Importantly, treating TPX2-overexpressing cells with the autophagy inhibitor chloroquine significantly reversed their enhanced migration, proliferation, and stemness marker expression.

Indexed as

autophagylung adenocarcinomatherapeutic targetTPX2tumor stemness

Identifiers

PMID42311261
PMCPMC13269291

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.