Evidence map›Paper›PMID 42611118›Full record

ArticleMolecular biology reports2026

PPIB interacts with MET to activate the PI3K-AKT pathway and promote head and neck squamous cell carcinoma pathogenesis.

Zhaobo Liu, Lin Wang, Jin Tang, Jingxuan Ran, Linsheng Dong, Yadong Li

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Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Zhaobo LiuDepartment of Oral and Maxillofacial Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Lin WangDepartment of Stomatology, School of Medicine, Yangpu Hospital, Tongji University, Shanghai, China.
Jin TangDepartment of Oral and Maxillofacial Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Jingxuan RanDepartment of Oral and Maxillofacial Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Linsheng DongDepartment of Oral and Maxillofacial Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Yadong LiDepartment of Oral and Maxillofacial Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China. llxxyydd2006@sina.com.

Funding

Graduate Research Innovation Project Foundation of Chongqing CYS22339Natural Science Foundation of Chongqing Municipality,China CSTB2023NSCQ-MSX0087
6 · The paper itself

Abstract

backgroundPeptidyl-prolyl isomerase B (PPIB) is involved in the occurrence and development of various malignant tumors, yet its clinical function and molecular mechanism in head and neck squamous cell carcinoma (HNSCC) remain unclear. This study aimed to explore the biological role and underlying molecular mechanism of PPIB in the malignant progression of HNSCC. METHODS AND

resultsCombined with bioinformatics analysis, immunohistochemistry, and Western blotting detection, this study confirmed that PPIB was significantly upregulated in HNSCC tissues and closely correlated with malignant pathological phenotypes and poor patient prognosis. In vitro functional experiments showed that PPIB promotes the proliferation, migration and invasion of HNSCC cells by regulating cell cycle distribution, cell apoptosis, and epithelial-mesenchymal transition-related molecules. In vivo xenograft and lung metastasis models further verified the oncogenic effect of PPIB. Transcriptome sequencing identified MET as a key downstream target of PPIB. Co-IP and immunofluorescence assays confirmed the interaction between PPIB and MET. Drug intervention and MET knockdown rescue experiments further demonstrated that PPIB interacts with MET to activate the PI3K-AKT signaling pathway, thereby facilitating the malignant progression of HNSCC.

conclusionsThis study confirms that PPIB activates the PI3K-AKT signaling pathway by interacting with MET, thereby promoting the malignant progression of HNSCC. PPIB has the potential to serve as a therapeutic target for HNSCC and deserves further in-depth research.

Indexed as

CyclophilinsHead and Neck NeoplasmsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-metSquamous Cell Carcinoma of Head and NeckAnimalsApoptosisCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansMalecyclophilin BCyclophilinsMET protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-methead and neck squamous cell carcinomaMETPI3K-AKT pathwayPPIB

Identifiers

PMID42611118

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