Evidence map›Paper›PMID 40659704›Full record

ArticleScientific reports2025

PLAGL2 as a prognostic biomarker and an EMT-promoting factor in PDAC.

Yan-Hui Yang, Hao Wang, Zhe-Hua Xing, Qian-Qian Bai, Wei-Feng Liu, Da-Huan Li, Chi Zhang, Shu-Min Zhang, Fang-Fei Liu, Yu-Bo Liu and 1 more

Abstract read
In one paragraph

Article in Scientific reports, 2025. 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

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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

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

11 authors.

Yan-Hui YangThe First Affiliated Hospital, and College of Clinical Medicine of Henan, University of Science and Technology, No. 24 Jing-Hua Road, Luoyang, 471003, Henan Province, China.
Hao WangThe First Affiliated Hospital, and College of Clinical Medicine of Henan, University of Science and Technology, No. 24 Jing-Hua Road, Luoyang, 471003, Henan Province, China.
Zhe-Hua XingThe First Affiliated Hospital, and College of Clinical Medicine of Henan, University of Science and Technology, No. 24 Jing-Hua Road, Luoyang, 471003, Henan Province, China.
Qian-Qian BaiThe First Affiliated Hospital, and College of Clinical Medicine of Henan, University of Science and Technology, No. 24 Jing-Hua Road, Luoyang, 471003, Henan Province, China.
Wei-Feng LiuThe First Affiliated Hospital, and College of Clinical Medicine of Henan, University of Science and Technology, No. 24 Jing-Hua Road, Luoyang, 471003, Henan Province, China.
Da-Huan LiThe First Affiliated Hospital, and College of Clinical Medicine of Henan, University of Science and Technology, No. 24 Jing-Hua Road, Luoyang, 471003, Henan Province, China.
Chi ZhangThe First Affiliated Hospital, and College of Clinical Medicine of Henan, University of Science and Technology, No. 24 Jing-Hua Road, Luoyang, 471003, Henan Province, China.
Shu-Min ZhangThe First Affiliated Hospital, and College of Clinical Medicine of Henan, University of Science and Technology, No. 24 Jing-Hua Road, Luoyang, 471003, Henan Province, China.
Fang-Fei LiuThe First Affiliated Hospital, and College of Clinical Medicine of Henan, University of Science and Technology, No. 24 Jing-Hua Road, Luoyang, 471003, Henan Province, China.
Yu-Bo LiuThe First Affiliated Hospital, and College of Clinical Medicine of Henan, University of Science and Technology, No. 24 Jing-Hua Road, Luoyang, 471003, Henan Province, China.
Hua FanThe First Affiliated Hospital, and College of Clinical Medicine of Henan, University of Science and Technology, No. 24 Jing-Hua Road, Luoyang, 471003, Henan Province, China. fanhua19851229@126.com.

Funding

2023 2302014Y
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC), the most prevalent form of pancreatic malignancy, is characterized by its aggressive nature and high mortality rate, with a 5-year survival rate in China of only 9.9%. Polymorphic adenoma gene-like 2 (PLAGL2) has been implicated in the development of various digestive tract tumors, including hepatocellular carcinoma, gastric carcinoma, and colorectal carcinoma, and it influences tumor progression through multiple pathways. However, the specific role and mechanism of PLAGL2 in PDAC requires further investigation. The objective of this study was to evaluate the expression level of PLAGL2 in PDAC and its association with clinical parameters, thereby assessing its prognostic significance for PDAC, and its impact on the malignant process. We first analyzed the expression of PLAGL2 in pancreatic ductal adenocarcinoma (PDAC) via multiple databases, including TCGA and GTEx, to investigate its associated enrichment pathways. We subsequently examined the expression of PLAGL2 via immunohistochemistry and PCR in PDAC tumor tissue samples from our hospital, explored the relationships between PLAGL2 expression and clinical features, and evaluated the predictive value of PLAGL2 for the survival of PDAC patients. we investigated the effect of PLAGL2 on the epithelial‒mesenchymal transition (EMT) process by examining its association with the expression of EMT-related proteins. Finally, We confirmed that PLAGL2 facilitates the proliferation, invasion, and migration of PDAC using conventional cellular assays. The immunohistochemistry and PCR results, combined with the results of GEPIA analysis, indicated that PLAGL2 was significantly overexpressed in patients with pancreatic ductal adenocarcinoma (PDAC). GO analysis revealed that PLAGL2 was intricately linked to protein modification and regulation, as well as nerve projection development. The KEGG and GSEA enrichment analyses indicated that several signaling pathways, including the PI3K-AKT pathway, were significantly enriched, particularly in relation to EMT. The characterization of PLAGL2 expression and its clinicopathological features indicated that high PLAGL2 expression was associated with poor prognosis in PDAC patients and was positively correlated with TNM stge, TNM: T,TNM: N, Tumor size, Nerve infiltration and other clinical characteristics of the tumor. Immunohistochemical analysis suggested that PLAGL2 plays a role in enhancing the epithelial-to-mesenchymal transition (EMT) process in PDAC. By knocking down or overexpressing PLAGL2 in PDAC cell lines and conducting a series of cellular experiments, we ultimately demonstrated that low expression of PLAGL2 inhibits proliferation, migration, and invasion in PDAC, while high expression of PLAGL2 promotes these processes. This study demonstrated that the expression level of PLAGL2 serves as a predictive biomarker for survival in patients with pancreatic ductal adenocarcinoma (PDAC). It is associated with clinical features, including TNM stge, Tumor size, Nerve infiltration, and it also plays a role in promoting epithelial‒mesenchymal transition (EMT) in PDAC, and promotes the proliferation, migration and invasion of PDAC.

Indexed as

Biomarkers, TumorCarcinoma, Pancreatic DuctalDNA-Binding ProteinsEpithelial-Mesenchymal TransitionPancreatic NeoplasmsTranscription FactorsAgedCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMaleMiddle AgedPrognosisBiomarkers, TumorDNA-Binding ProteinsPLAGL2 protein, humanRNA-Binding ProteinsTranscription FactorsBiomarkerEMTPDACPLAGL2

Identifiers

PMID40659704
PMCPMC12260021

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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.