Evidence map›Paper›PMID 37924160›Full record

ArticleBiology direct2023

LY6/PLAUR domain containing 3 (LYPD3) maintains melanoma cell stemness and mediates an immunosuppressive microenvironment.

Yi-Dou Hu, Ke Wu, Yuan-Jie Liu, Qian Zhang, Hui Shen, Jin Ji, Dong Fang, Song-Yang Xi

Open access · goldAbstract read
In one paragraph

Article in Biology direct, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

9 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Exploring the molecular function of LYPD3 from pan-cancer to lung cancer: based on bioinformatics and cellular experiments.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Article
  3. Article
  4. Review
  5. Article
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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

8 authors at 2 institutions in 1 country.

Yi-Dou Hu *Zhangjiagang TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Zhangjiagang, 215600, Jiangsu, People's Republic of China.
Ke Wu *The Second Affiliated Hospital of Soochow University, Suzhou, 215004, Jiangsu, People's Republic of China.
Yuan-Jie LiuNo. 1 Clinical Medical College, Nanjing University of Chinese Medicine, Nanjing, 210023, Jiangsu, People's Republic of China.
Qian ZhangNo. 1 Clinical Medical College, Nanjing University of Chinese Medicine, Nanjing, 210023, Jiangsu, People's Republic of China.
Hui ShenZhangjiagang TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Zhangjiagang, 215600, Jiangsu, People's Republic of China.
Jin JiNanjing University of Chinese Medicine, Jiangsu Province Hospital of Chinese Medicine, Nanjing, 210029, Jiangsu, People's Republic of China.
Dong FangZhenjiang Hospital of Chinese Traditional and Western Medicine, Zhenjiang, Jiangsu, 212000, People's Republic of China. fdzjszxyjhyy@163.com.
Song-Yang XiNo. 1 Clinical Medical College, Nanjing University of Chinese Medicine, Nanjing, 210023, Jiangsu, People's Republic of China. 20215011@njucm.edu.cn.
Nanjing University of Chinese Medicine · CNSecond Affiliated Hospital of Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMalignant melanoma is a highly heterogeneous skin cancer with the highest mortality rate among dermatological cancers. Catenins form functional networks in the nucleus to regulate gene expression and determine cell fate. Dysregulation of catenin expression correlates with the malignant characteristics of the tumor. We aimed to investigate the regulatory mechanisms of catenins in melanoma and to further define the function of catenin-related molecular signaling in the tumor microenvironment.

methodsIn this study, a bioinformatics approach combined with experimental validation was used to explore the potential tumor biology mechanisms of catenin-related signaling.

resultsMelanoma patients can be divided into two catenin clusters. Patients defined by high Junction Plakoglobin (JUP), Plakophilin 1 (PKP1), Plakophilin 3 (PKP3) levels (C2) had shorter survival time than other patients (C1). We demonstrated that JUP regulates Anterior Gradient 2 (AGR2)/LY6/PLAUR Domain Containing 3 (LYPD3) to maintain melanoma stemness and promotes glycolysis. We also found that LYPD3 was co-expressed with S100A9 and associated with immunosuppressive tumor microenvironment (TME).

conclusionThe JUP/AGR2/LYPD3 signaling axis plays an important role in the malignant features of melanoma. Targeting the JUP/AGR2/LYPD3 signaling axis can help develop promising drugs.

Indexed as

Cell Adhesion MoleculesGPI-Linked ProteinsMelanomaSkin NeoplasmsCateninsHumansMucoproteinsOncogene ProteinsSignal TransductionTumor MicroenvironmentAGR2 protein, humanCateninsCell Adhesion MoleculesGPI-Linked ProteinsLYPD3 protein, humanMucoproteinsOncogene ProteinsCancer stem cellCateninGlycolysisImmunotherapyLYPD3Melanoma

Identifiers

PMID37924160
PMCPMC10623712
OpenAlexW4388294725

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.