Transthyretin Suppressed Tumor Progression in Non‑Small Cell Lung Cancer by Inactivating MAPK/ERK Pathway
Overexpression of transthyretin (TTR) inhibits proliferation, migration and invasion of NSCLC cells and promotes apoptosis through suppression of the MAPK/ERK signaling pathway, thereby reducing tumor growth in vivo.
The study examined the role of transthyretin (TTR) in non‑small cell lung cancer (NSCLC) by modulating its expression in cell lines and animal models. TTR over‑expression markedly reduced NSCLC cell proliferation, migration and invasion while enhancing apoptosis. Western blot analyses revealed significant down‑regulation of phosphorylated ERK, indicating that TTR exerts its antitumor effect via inhibition of the MAPK/ERK pathway. In vivo experiments confirmed that TTR over‑expression suppresses tumor growth.
Identifying TTR as a negative regulator of NSCLC progression provides a novel biomarker and potential therapeutic target for improving diagnosis and treatment strategies in lung cancer.
Bizonyítékszint: Korai humán adat. Kis vagy feltáró emberi adat.
Kapcsolódó jelek
- Telisotuzumab Vedotin + Osimertinib for Non‑Small Cell Lung Cancer
- Ramucirumab plus erlotinib in patients with untreated, EGFR‑mutated, advanced non‑small‑cell lung cancer (RELAY): a randomised, double‑blind, placebo‑controlled, phase 3 trial
- Recent advancements in lung cancer research: a narrative review
- Advances in Non-Small Cell Lung Cancer: Current Insights and Future Directions
- Structured proxy features for multimodal NSCLC survival prediction from pretreatment CT