USP8-mediated PTK7 promotes PIK3CB-related pathway to accelerate the malignant progression of non-small cell lung cancer
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View abstract on PubMed
Summary
This summary is machine-generated.Ubiquitin-specific peptidase 8 (USP8) deubiquitinates and stabilizes protein tyrosine kinase 7 (PTK7), promoting non-small cell lung cancer (NSCLC) progression via the PIK3CB/PI3K/AKT pathway.
Area Of Science
- Oncology
- Molecular Biology
- Cancer Research
Background
- Protein tyrosine kinase 7 (PTK7) is highly expressed in non-small cell lung cancer (NSCLC).
- The precise molecular mechanisms underlying PTK7's role in NSCLC require further elucidation.
Purpose Of The Study
- To investigate the molecular mechanism of PTK7 in NSCLC progression.
- To explore the relationship between PTK7, ubiquitin-specific peptidase 8 (USP8), and the PI3K/AKT pathway in NSCLC.
Main Methods
- Quantitative real-time PCR and western blot to assess PTK7, USP8, and PIK3CB expression.
- Flow cytometry to evaluate macrophage M2 polarization.
- Co-immunoprecipitation (Co-IP) assays to determine protein interactions.
- In vivo animal studies to assess the effect of PTK7 and PIK3CB on NSCLC tumorigenesis.
Main Results
- PTK7 expression was elevated in NSCLC tissues and cells.
- PTK7 silencing inhibited NSCLC cell proliferation and invasion, promoted apoptosis, and reduced M2 polarization.
- USP8 enhanced PTK7 protein levels via deubiquitination, and USP8 knockdown effects were reversed by PTK7 overexpression.
- PTK7 interacted with PIK3CB, and PIK3CB overexpression counteracted PTK7 silencing effects.
- USP8, via PTK7, positively regulated PIK3CB, activating the PI3K/AKT pathway, leading to reduced NSCLC tumorigenesis upon PTK7 downregulation.
Conclusions
- USP8-stabilized PTK7 promotes NSCLC malignancy by activating the PIK3CB/PI3K/AKT pathway.
- This pathway presents a potential therapeutic target for NSCLC treatment.
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