Evidence map›Paper›PMID 42001899›Full record

ArticleCancer reports (Hoboken, N.J.)2026

CHI3L1 Is Associated With TP53 Signaling and Promotes Papillary Thyroid Carcinoma Progression.

Fen Cai, Ya'nan Zhou, Yeran Yang, Meng Zhang, Xuan Zhang, Yan Chang, Shengcai Wang, Xinyuan Wu, Yongli Guo, Yongbo Yu and 2 more

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PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer reports (Hoboken, N.J.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Fen CaiDepartment of Otolaryngology, Head and Neck Surgery, Hebei Children's Hospital, Hebei Medical University, Shijiazhuang, Hebei, China.
Ya'nan ZhouBeijing Key Laboratory for Pediatric Diseases of Otolaryngology, Head and Neck Surgery, MOE Key Laboratory of Major Diseases in Children, Beijing Pediatric Research Institute, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health (NCCH), Beijing, China.
Yeran YangBeijing Key Laboratory for Pediatric Diseases of Otolaryngology, Head and Neck Surgery, MOE Key Laboratory of Major Diseases in Children, Beijing Pediatric Research Institute, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health (NCCH), Beijing, China.
Meng ZhangDepartment of Pathology, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health (NCCH), Beijing, China.ORCID 0000-0003-1852-0322
Xuan ZhangBeijing Key Laboratory for Pediatric Diseases of Otolaryngology, Head and Neck Surgery, MOE Key Laboratory of Major Diseases in Children, Beijing Pediatric Research Institute, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health (NCCH), Beijing, China.
Yan ChangBeijing Key Laboratory for Pediatric Diseases of Otolaryngology, Head and Neck Surgery, MOE Key Laboratory of Major Diseases in Children, Beijing Pediatric Research Institute, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health (NCCH), Beijing, China.
Shengcai WangDepartment of Otolaryngology, Head and Neck Surgery, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health (NCCH), Beijing, China.
Xinyuan WuBeijing Key Laboratory for Pediatric Diseases of Otolaryngology, Head and Neck Surgery, MOE Key Laboratory of Major Diseases in Children, Beijing Pediatric Research Institute, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health (NCCH), Beijing, China.
Yongli GuoBeijing Key Laboratory for Pediatric Diseases of Otolaryngology, Head and Neck Surgery, MOE Key Laboratory of Major Diseases in Children, Beijing Pediatric Research Institute, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health (NCCH), Beijing, China.
Yongbo YuBeijing Key Laboratory for Pediatric Diseases of Otolaryngology, Head and Neck Surgery, MOE Key Laboratory of Major Diseases in Children, Beijing Pediatric Research Institute, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health (NCCH), Beijing, China.ORCID 0000-0002-2717-4073
Xin NiBeijing Key Laboratory for Pediatric Diseases of Otolaryngology, Head and Neck Surgery, MOE Key Laboratory of Major Diseases in Children, Beijing Pediatric Research Institute, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health (NCCH), Beijing, China.
Jiangqiao GengDepartment of Otolaryngology, Head and Neck Surgery, Hebei Children's Hospital, Hebei Medical University, Shijiazhuang, Hebei, China.

Funding

Beijing Research Ward Excel lence Program BRWEP2024W102090103Hebei Province 3-3-3 Talent Project Funding Project A202105016Key subjects of medical science research in Hebei Province 2022180
6 · The paper itself

Abstract

backgroundPapillary thyroid carcinoma (PTC) is the most commonly diagnosed subtype of thyroid cancer and represents a highly prevalent form of endocrine malignancy.

aimsThis study aimed to investigate the role and molecular mechanism of CHI3L1 in PTC progression. METHODS AND

resultsCHI3L1 expression in PTC was analyzed using public datasets. Cell proliferation was assessed using the CCK-8 assay and colony formation assay. Tumor growth was evaluated using nude mouse xenograft models. Cell invasion was evaluated using the transwell assay, while cell migration was assessed with the wound healing assay. Transcriptomic analysis was conducted to examine the molecular mechanism, and real-time quantitative PCR was performed for gene expression validation. The findings revealed that CHI3L1 expression was upregulated in various cancers, mainly in PTC. Both in vitro and in vivo assays demonstrated that cell proliferation was suppressed when CHI3L1 was knocked down. Transcriptome sequencing indicated that CHI3L1 knockdown was associated with migration-related pathways and the TP53 signaling pathway. Transwell assays showed reduced cell invasion upon CHI3L1 suppression, while wound healing assays demonstrated decreased cell migration. Following CHI3L1 silencing, real-time quantitative PCR verified the overexpression of TP53-related genes. Survival analysis further indicated a correlation between elevated CHI3L1 expression and reduced survival rates.

conclusionThis study identified that CHI3L1 was an oncogene in PTC and promotes tumor cell proliferation associated with downregulating the TP53 pathway. It provides new evidence supporting CHI3L1 as a potential molecular target for future therapeutic investigation in PTC.

Indexed as

Chitinase-3-Like Protein 1Thyroid Cancer, PapillaryThyroid NeoplasmsTumor Suppressor Protein p53AnimalsCell Line, TumorCell MovementCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMiceMice, NudeSignal TransductionCHI3L1 protein, humanChitinase-3-Like Protein 1TP53 protein, humanTumor Suppressor Protein p53CHI3L1migrationpapillary thyroid carcinomaproliferationTP53 pathway

Identifiers

PMID42001899
PMCPMC13092342

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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.