Evidence map›Paper›PMID 40954243›Full record

ArticleJournal of cancer research and clinical oncology2025

PPARγ accelerates OSCC progression via Th17 polarization and CEBPA/IL-17C signaling.

Ying Wang, Jing Liang, Shiyu Zhang, Yingxin Zhang, Fangbu Cheng, Ning Ji, Jing Li, Qianming Chen, Xin Zeng

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cancer research and clinical oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 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

9 authors.

Ying Wang *State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Research Unit of Oral Carcinogenesis and Management, Chinese Academy of Medical Sciences, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Jing Liang *State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Research Unit of Oral Carcinogenesis and Management, Chinese Academy of Medical Sciences, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Shiyu Zhang *State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Research Unit of Oral Carcinogenesis and Management, Chinese Academy of Medical Sciences, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Yingxin ZhangState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Research Unit of Oral Carcinogenesis and Management, Chinese Academy of Medical Sciences, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Fangbu ChengState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Research Unit of Oral Carcinogenesis and Management, Chinese Academy of Medical Sciences, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Ning JiState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Research Unit of Oral Carcinogenesis and Management, Chinese Academy of Medical Sciences, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Jing LiState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Research Unit of Oral Carcinogenesis and Management, Chinese Academy of Medical Sciences, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Qianming ChenState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Research Unit of Oral Carcinogenesis and Management, Chinese Academy of Medical Sciences, West China Hospital of Stomatology, Sichuan University, Chengdu, China. qmchen@scu.edu.cn.
Xin ZengState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Research Unit of Oral Carcinogenesis and Management, Chinese Academy of Medical Sciences, West China Hospital of Stomatology, Sichuan University, Chengdu, China. zengxin22@163.com.

Funding

the CAMS Innovation Fund for Medical Sciences 2019-I2 M-5-004the National Natural Science Foundation of China 82072999the National Natural Science Foundation of China 82270986
6 · The paper itself

Abstract

backgroundOral squamous cell carcinoma (OSCC) is a marked invasive epithelial tumor with limited treatment efficacy, especially in advanced stages. The immunosuppressive nature of the tumor microenvironment (TME) is a major contributor to OSCC development and therapeutic resistance. Peroxisome proliferator-activated receptor gamma (PPARγ) is known to influence tumor biology in a multifaceted and context-specific manner. The objective of this research was to explore the role of PPARγ in modulating the TME and its impact on OSCC progression.

methodsA 4NQO-induced OSCC model was used to verify PPARγ overexpression by Immunohistochemistry (IHC). Bulk RNA-seq and single-cell RNA-seq analyses were employed to dissect PPARγ-driven tumor-promoting mechanisms. Co-cultivation of OSCC cells and CD4 + T cells in vitro, combined with subcutaneous tumor model in vivo, was employed to investigate the influence of PPARγ on Th17 cells differentiation.

resultsInhibition of PPARγ significantly suppressed OSCC cell growth and downregulated IL-17 pathway-related genes, including IL-17C. PPARγ promoted Th17 cells differentiation via transcriptional upregulation of CEBPA/IL-17C/IL-17A signaling pathway. Evidence from cell-based and animal experiments confirmed that GW9662 treatment impaired Th17 cells polarization and reduced expression of CEBPA, IL-17C, and IL-17A.

conclusionThis study identifies a novel PPARγ/CEBPA/IL-17C/IL-17A signaling axis that promotes Th17 differentiation and contributes to tumor-associated inflammation in OSCC. Targeting PPARγ represents a promising strategy to inhibit tumor progression and modulate the immune microenvironment, providing new insight into immunotherapeutic approaches for OSCC.

Indexed as

Carcinoma, Squamous CellInterleukin-17Mouth NeoplasmsPPAR gammaSquamous Cell Carcinoma of Head and NeckTh17 CellsAnimalsCell DifferentiationCell Line, TumorDisease ProgressionHumansMiceSignal TransductionTumor MicroenvironmentInterleukin-17PPAR gammaPPARG protein, humanCEBPAIL-17OSCCPPARγTh17 cellsTME

Identifiers

PMID40954243
PMCPMC12436265

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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 OpenQuestion graph.