Evidence map›Paper›PMID 41844740›Full record

ArticleScientific reports2026

CHD1L promotes testicular cancer progression through epigenetic activation of the CXCR6/PI3K/AKT pathway.

Yang Zhao, Hao Yan, Xinda Chen, Xiaolin Zhang, Mujun Lu, Ming Zhang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2026. 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. 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

6 authors.

Yang Zhao *Department of Urology, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Hao Yan *Department of Urology, Fudan University Shanghai Cancer Center, Shanghai, China.
Xinda ChenDepartment of Urology and Andrology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Xiaolin ZhangDepartment of Urology and Andrology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Mujun LuDepartment of Urology and Andrology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. lumujun@renji.com.
Ming ZhangDepartment of Urology and Andrology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. zhangming7185@renji.com.

Funding

National Key Research and Development Program of China 2022YFC2804300National Natural Science Foundation of China-China Academy of General Technology Joint Fund for Basic Research 82171611, 81971376Shanghai Science and Technology Commission Research Project 21ZR14389001
6 · The paper itself

Abstract

Testicular cancer is the most common malignancy in young men, and treatment options for metastatic or refractory disease remain limited. Chromatin remodeling plays a critical role in tumorigenesis, yet its contribution to testicular cancer progression is poorly understood. This study aimed to elucidate the oncogenic and epigenetic functions of chromodomain helicase DNA-binding protein 1-like (CHD1L) in testicular cancer. Immunohistochemistry and TCGA transcriptomic analyses were performed to assess CHD1L expression and clinical relevance. Functional assays, RNA sequencing, and ATAC-seq were conducted to explore its biological effects and regulatory mechanisms. In vivo xenograft models were used to validate tumor-promoting activity. CHD1L was markedly overexpressed in testicular cancer tissues and correlated with advanced pathological stage. High CHD1L expression was correlated with immune-infiltration patterns indicative of immune exclusion, including increased Treg/Th2 signatures and reduced cytotoxic T-cell activity based on TCGA analyses. Functional studies revealed that CHD1L enhanced cell proliferation, migration, and invasion both in vitro and in vivo. Integrative multi-omics analyses identified CXCR6 as a direct downstream effector of CHD1L. Mechanistically, CHD1L promoted CXCR6 transcription through H3K9me3 demethylation, thereby activating the PI3K/AKT signaling pathway. CHD1L drives testicular cancer progression through epigenetic activation of the CXCR6/PI3K/AKT axis and immune modulation. These findings highlight CHD1L as a potential therapeutic target for advanced or treatment-resistant testicular cancer.

Indexed as

DNA-Binding ProteinsDNA HelicasesEpigenesis, GeneticPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, CXCR6Testicular NeoplasmsAnimalsCell Line, TumorCell MovementCell ProliferationDisease ProgressionGene Expression Regulation, NeoplasticHumansMaleMiceDNA-Binding ProteinsDNA HelicasesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, CXCR6CHD1LCXCR6Immune microenvironmentTesticular cancerTumor progression

Identifiers

PMID41844740
PMCPMC13133128

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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.