Evidence map›Paper›PMID 39468431›Full record

ArticleMolecular medicine (Cambridge, Mass.)2024

Deciphering STAT3's negative regulation of LHPP in ESCC progression through single-cell transcriptomics analysis.

Yurao Chen, Zemao Zheng, Luoshai Wang, Ronghuai Chen, Ming He, Xiang Zhao, Liyan Jin, Juan Yao

Abstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2024. 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

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

1 citing paper in PubMed.

  1. Identification ofInternational journal of molecular sciences · 2025
    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

8 authors.

Yurao Chen *Department of Radiation Oncology, Huaian Hospital of Huaian City, Huaian, 223299, Jiangsu, China.
Zemao Zheng *Department of Radiation Oncology, Huaian Hospital of Huaian City, Huaian, 223299, Jiangsu, China.
Luoshai Wang *Department of Thoracic Surgery, Huaian Hospital of Huaian City, Huaian, 223299, Jiangsu, China.
Ronghuai ChenDepartment of Radiation Oncology, Huaian Hospital of Huaian City, Huaian, 223299, Jiangsu, China.
Ming HeDepartment of Radiation Oncology, Huaian Hospital of Huaian City, Huaian, 223299, Jiangsu, China.
Xiang ZhaoDepartment of Radiation Oncology, Huaian Hospital of Huaian City, Huaian, 223299, Jiangsu, China.
Liyan JinDepartment of Oncology, Wujin Hospital Affiliated with Jiangsu University, Changzhou, 213000, Jiangsu, China. jinliyan@wjrmyy.cn.
Juan YaoDepartment of Radiation Oncology, Huaian Hospital of Huaian City, Huaian, 223299, Jiangsu, China. tzsry110120@163.com.

Funding

Scientific research project of Jiangsu Provincial Health Commission Z2022084
6 · The paper itself

Abstract

backgroundEsophageal Squamous Cell Carcinoma (ESCC) remains a predominant health concern in the world, characterized by high prevalence and mortality rates. Advances in single-cell transcriptomics have revolutionized cancer research by enabling a precise dissection of cellular and molecular diversity within tumors.

objectiveThis study aims to elucidate the cellular dynamics and molecular mechanisms in ESCC, focusing on the transcriptional influence of STAT3 (Signal Transducer and Activator of Transcription 3) and its interaction with LHPP, thereby uncovering potential therapeutic targets.

methodsSingle-cell RNA sequencing was employed to analyze 44,206 cells from tumor and adjacent normal tissues of ESCC patients, identifying distinct cell types and their transcriptional shifts. We conducted differential gene expression analysis to assess changes within the tumor microenvironment (TME). Validation of key regulatory interactions was performed using qPCR in a cohort of 21 ESCC patients and further substantiated through experimental assays in ESCC cell lines.

resultsThe study revealed critical alterations in cell composition and gene expression across identified cell populations, with a notable shift towards pro-tumorigenic states. A significant regulatory influence of STAT3 on LHPP was discovered, establishing a novel aspect of ESCC pathogenesis. Elevated levels of STAT3 and suppressed LHPP expression were validated in clinical samples. Functional assays confirmed that STAT3 directly represses LHPP at the promoter level, and disruption of this interaction by promoter mutations diminished STAT3's repressive effect.

conclusionThis investigation underscores the central role of STAT3 as a regulator in ESCC, directly impacting LHPP expression and suggesting a regulatory loop crucial for tumor behavior. The insights gained from our comprehensive cellular and molecular analysis offer a deeper understanding of the dynamics within the ESCC microenvironment. These findings pave the way for targeted therapeutic interventions focusing on the STAT3-LHPP axis, providing a strategic approach to improve ESCC management and prognosis.

Indexed as

Esophageal NeoplasmsEsophageal Squamous Cell CarcinomaGene Expression Regulation, NeoplasticSingle-Cell AnalysisSTAT3 Transcription FactorTumor MicroenvironmentCell Line, TumorDisease ProgressionGene Expression ProfilingHumansTranscriptomeSTAT3 protein, humanSTAT3 Transcription FactorESCCLHPPSingle-cell transcriptomicsSTAT3Tumor microenvironment

Identifiers

PMID39468431
PMCPMC11520558

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.