ArticleThoracic cancer2025
USP8-mediated PTK7 promotes PIK3CB-related pathway to accelerate the malignant progression of non-small cell lung cancer.
Article in Thoracic cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Pathological role of deubiquitinating enzymes in lung cancer: recent insights and advances.American journal of cancer research · 2026Review
- Deciphering USP8's pivotal role in cancer: mechanisms, clinical insights and contrasts with its function in pituitary adenomas.Journal of translational medicine · 2025Review
- USP8-mediated PTK7 promotes PIK3CB-related pathway to accelerate the malignant progression of non-small cell lung cancer.Thoracic cancer · 2025Article
- Berberine in the treatment of radiation-induced skin injury: insights from proteomics and network pharmacology.Frontiers in pharmacology · 2025Article
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Authors and funding
5 authors.
Funding
Abstract
backgroundProtein tyrosine kinase 7 (PTK7) has been found to be highly expressed in non-small cell lung cancer (NSCLC), but its specific molecular mechanism needs to be further explored.
methodsPTK7 mRNA expression in NSCLC tumor tissues was examined by quantitative real-time PCR. The protein levels of PTK7, ubiquitin-specific peptidase 8 (USP8), PIK3CB, and PI3K/AKT were determined by western blot. Human monocytes (THP-1) were induced into macrophages and then co-cultured with the conditioned medium of NSCLC cells. Macrophage M2 polarization was assessed by detecting CD206
resultsPTK7 expression was higher in NSCLC tumor tissues and cells. After silencing of PTK7, NSCLC cell proliferation, invasion, and macrophage M2 polarization were inhibited, while cell apoptosis was promoted. USP8 enhanced PTK7 protein expression by deubiquitination, and the repressing effects of USP8 knockdown on NSCLC cell growth, invasion, and macrophage M2 polarization were reversed by PTK7 overexpression. PTK7 interacted with PIK3CB, and PIK3CB overexpression could abolish the regulation of PTK7 silencing on NSCLC cell progression. USP8 positively regulated PIK3CB expression by PTK7, thus activating PI3K/AKT pathway. Downregulation of PTK7 reduced NSCLC tumorigenesis by decreasing PIK3CB expression.
conclusionUSP8-deubiquitinated PTK7 facilitated NSCLC malignant behavior via activating the PIK3CB/PI3K/AKT pathway, providing new idea for NSCLC treatment.
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