Evidence map›Paper›PMID 40410851›Full record

ArticleJournal of translational medicine2025

S1PR3 inhibition impairs cell cycle checkpoint via the AKT/WEE1 pathway in oral squamous cell carcinoma.

Xinxia Zhou, Jinghao Liu, Xu Chen, Xinyu Zhou, Beihui Xu, Guifang Gan, Fuxiang Chen

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of translational medicine, 2025. 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
–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

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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

3 citing papers in PubMed.

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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.

Xinxia ZhouDepartment of Clinical Immunology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200011, China.
Jinghao LiuDepartment of Clinical Immunology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200011, China.
Xu ChenDepartment of Clinical Immunology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200011, China.
Xinyu ZhouDepartment of Oral and Maxillofacial-Head and Neck Oncology, College of Stomatology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Beihui XuDepartment of Clinical Immunology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200011, China.
Guifang GanDepartment of Clinical Immunology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200011, China. agan1992@126.com.
Fuxiang ChenDepartment of Clinical Immunology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200011, China. chenfx@sjtu.edu.cn.ORCID 0000-0002-4093-2676

Funding

Fundamental Research Funds for the Central Universities YG2022QN065Fundamental Research Program Funding of the Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine JYJC202227National Key Research and Development Program 2023YFB3210305National Natural Science Foundation of China 81870762National Natural Science Foundation of China 82203551Shanghai Municipal Commission of Health and Family Planning 20244Y0193
6 · The paper itself

Abstract

backgroundSphingosine-1-phosphate receptor 3 (S1PR3) has been implicated in promoting tumor progression in various cancers. However, the role and molecular mechanisms of S1PR3 in oral squamous cell carcinoma (OSCC) remain poorly understood. The aims of this study were to investigate the function of S1PR3 in OSCC progression and its potential as a therapeutic target.

methodThe expression of S1PR3 was determined through qPCR, Western blotting analysis, immunohistochemistry (IHC), and the TCGA database. The correlation between S1PR3 expression and clinical prognosis was analyzed using the TCGA database and IHC. The effects of S1PR3 on OSCC cell proliferation and cell cycle were investigated through CCK-8 assay, colony formation assay, EdU incorporation assay, cell cycle analysis, and a xenograft mouse model. The potential mechanisms through which S1PR3 affects the OSCC cell cycle were explored using RNA-seq and a cell cycle array. The effects of combining S1PR3 antagonist with cisplatin on OSCC cell growth were examined through CCK-8 and EdU incorporation assays.

resultsS1PR3 was overexpressed in OSCC and the upregulation of S1PR3 in OSCC was correlated with unfavorable clinicopathological characteristics and adverse prognosis. Targeting S1PR3 reduced AKT phosphorylation, which led to a downregulation of WEE1, a kinase involved in cell cycle regulation. This downregulation resulted in reducing CDC2 phosphorylation, disrupting the G2/M cell cycle checkpoint and inhibiting OSCC cell proliferation. Furthermore, the combination of S1PR3 antagonist exhibited synergistic inhibitory effects on OSCC cell growth when combined with cisplatin.

conclusionsThese findings reveal a critical role for S1PR3 in regulating OSCC cell cycle via the AKT/WEE1/CDC2 pathway, thus offering a basis for developing treatment strategies for OSCC patients.

Indexed as

Carcinoma, Squamous CellCell Cycle CheckpointsCell Cycle ProteinsMouth NeoplasmsProto-Oncogene Proteins c-aktSignal TransductionSphingosine-1-Phosphate ReceptorsAnimalsCell Line, TumorCell ProliferationCisplatinFemaleGene Expression Regulation, NeoplasticHumansMaleMiceCell Cycle ProteinsCisplatinProto-Oncogene Proteins c-aktsphingosine-1-phosphate receptor-3, humanSphingosine-1-Phosphate ReceptorsAKT signaling pathwayCell cycleOral squamous cell carcinomaSphingosine-1-phosphate receptor 3WEE1

Identifiers

PMID40410851
PMCPMC12102893

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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.