TMEM176B Promotes EMT via FGFR/JNK Signalling in Development and Tumourigenesis of Lung Adenocarcinoma
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View abstract on PubMed
Summary
This summary is machine-generated.TMEM176B is elevated in lung adenocarcinoma, promoting cancer growth and spread. Targeting TMEM176B offers a potential new therapeutic strategy for lung cancer patients.
Area Of Science
- Oncology
- Molecular Biology
- Cancer Research
Background
- Lung cancer is a leading global cause of cancer mortality with poor prognosis.
- Novel therapeutic targets are crucial for treating inoperable metastatic lung cancer.
- TMEM176B has been identified as a potential therapeutic target in other cancers.
Purpose Of The Study
- To investigate the role of TMEM176B in the development of lung adenocarcinoma.
- To explore TMEM176B as a potential therapeutic target for lung adenocarcinoma.
Main Methods
- Single-cell sequencing
- Proteomics
- Co-immunoprecipitation (Co-IP)
- In vivo and in vitro experimental models
Main Results
- TMEM176B expression is increased in lung adenocarcinoma tissues and linked to shorter overall survival.
- TMEM176B enhances cancer cell proliferation, invasion, migration, and adhesion in vitro, and tumor growth in vivo.
- TMEM176B promotes endothelial cell tube formation and regulates epithelial-mesenchymal transition (EMT) via the FGFR1/JNK/Vimentin/Snail pathway.
Conclusions
- TMEM176B plays a significant role in lung adenocarcinoma progression.
- TMEM176B represents a promising therapeutic target for lung adenocarcinoma treatment.
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