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

BACKGROUND

Peptidyl-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

RESULTS

Combined 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.

CONCLUSIONS

This 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.