Evidence map›Paper›PMID 40944975›Full record

ArticleTranslational oncology2025

FAP promotes progression of oral leukoplakia via activation of PI3K/AKT pathway by interacting with ITGB1.

Ran Li, Tiantian Liu, Yixuan Gu, Yuantao Gao, Xiaofeng Jiao, Yanwei Li, Songqingmeng Tian, Kejie Cao

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Translational oncology, 2025. 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. Review
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.

Ran LiShanxi Medical University School and Hospital of Stomatology, Shanxi Province Key Laboratory of Oral Diseases Prevention and New Materials, Clinical Research Center of Shanxi Province, Clinical Medical Research Center for Oral Diseases (Maxillofacial Deformities), Taiyuan 030001, China; Department of Oral Preventive Health, Shanxi Medical University School and Hospital of Stomatology, Taiyuan, Shanxi 030001, China. Electronic address: lraner@163.com.
Tiantian LiuShanxi Medical University School and Hospital of Stomatology, Shanxi Province Key Laboratory of Oral Diseases Prevention and New Materials, Clinical Research Center of Shanxi Province, Clinical Medical Research Center for Oral Diseases (Maxillofacial Deformities), Taiyuan 030001, China; Department of Oral Preventive Health, Shanxi Medical University School and Hospital of Stomatology, Taiyuan, Shanxi 030001, China.
Yixuan GuShanxi Medical University School and Hospital of Stomatology, Shanxi Province Key Laboratory of Oral Diseases Prevention and New Materials, Clinical Research Center of Shanxi Province, Clinical Medical Research Center for Oral Diseases (Maxillofacial Deformities), Taiyuan 030001, China; Department of Oral Preventive Health, Shanxi Medical University School and Hospital of Stomatology, Taiyuan, Shanxi 030001, China.
Yuantao GaoDepartment of Otorhinolaryngology Head and Neck Surgery, the Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou 310052, China.
Xiaofeng JiaoShanxi Medical University School and Hospital of Stomatology, Shanxi Province Key Laboratory of Oral Diseases Prevention and New Materials, Clinical Research Center of Shanxi Province, Clinical Medical Research Center for Oral Diseases (Maxillofacial Deformities), Taiyuan 030001, China; Department of Oral Preventive Health, Shanxi Medical University School and Hospital of Stomatology, Taiyuan, Shanxi 030001, China.
Yanwei LiShanxi Medical University School and Hospital of Stomatology, Shanxi Province Key Laboratory of Oral Diseases Prevention and New Materials, Clinical Research Center of Shanxi Province, Clinical Medical Research Center for Oral Diseases (Maxillofacial Deformities), Taiyuan 030001, China; Department of Oral Preventive Health, Shanxi Medical University School and Hospital of Stomatology, Taiyuan, Shanxi 030001, China.
Songqingmeng TianShanxi Medical University School and Hospital of Stomatology, Shanxi Province Key Laboratory of Oral Diseases Prevention and New Materials, Clinical Research Center of Shanxi Province, Clinical Medical Research Center for Oral Diseases (Maxillofacial Deformities), Taiyuan 030001, China; Department of Oral Preventive Health, Shanxi Medical University School and Hospital of Stomatology, Taiyuan, Shanxi 030001, China.
Kejie CaoShanxi Medical University School and Hospital of Stomatology, Shanxi Province Key Laboratory of Oral Diseases Prevention and New Materials, Clinical Research Center of Shanxi Province, Clinical Medical Research Center for Oral Diseases (Maxillofacial Deformities), Taiyuan 030001, China; Department of Oral Preventive Health, Shanxi Medical University School and Hospital of Stomatology, Taiyuan, Shanxi 030001, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThis study aims to elucidate the molecular mechanisms by which fibroblast activation protein (FAP) contributes to the malignant progression of oral leukoplakia (OLK).

methodsFAP expression was assessed via immunohistochemistry in human OLK and oral squamous cell carcinoma (OSCC) tissues across varying grades of dysplasia (mild, moderate, and severe). DOK and SCC15 cell lines were transfected to modulate FAP expression, followed by functional assays including colony formation, cell viability, transwell migration, and wound healing. Western blot analysis was performed to evaluate the expression of proteins involved in the integrin β1 (ITGB1) /PI3K/AKT pathway. In vivo, FAP-knockdown reagents were administered to OLK lesions in a murine model. Hematoxylin and eosin (HE) staining was used to assess the incidence of dysplasia and OSCC, while immunohistochemistry (IHC) was employed to examine FAP and p-AKT expression.

resultsFAP and p-AKT expression levels were positively correlated with the severity of dysplasia in OLK. Mechanistic investigations revealed that FAP enhances malignant behaviors such as proliferation and migration through activation of the ITGB1/PI3K/AKT signaling pathway. Importantly, suppression of FAP significantly reduced the incidence of both oral epithelial dysplasia and OSCC in the mouse model.

conclusionFAP facilitates the progression of OLK via the ITGB1/PI3K/AKT signaling axis, and its suppression attenuates malignant transformation. CLINICAL SIGNIFICANCE: This study highlights the critical involvement of FAP in the malignant transformation of OLK, offering new theoretical foundations for early diagnosis and targeted intervention. The expression level of FAP is positively correlated with the degree of OLK dysplasia, indicating its potential utility as a biomarker for evaluating malignant transformation risk. Moreover, therapeutic approaches targeting FAP or the ITGB1/PI3K/AKT signaling pathway may delay or prevent the progression of OLK to OSCC, presenting promising avenues for the development of precision medicine strategies in clinical practice.

Indexed as

Fibroblast activation proteinIntegrin β1Oral leukoplakiaOral squamous cell carcinomaPI3K/AKT pathway

Identifiers

PMID40944975
PMCPMC12496239

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