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Apatinib inhibits macrophage-mediated epithelial-mesenchymal transition in lung cancer
Shuliang Liu1, Lingfei Su2, Xuri Mu1
1Department of Thoracic Surgery, Yantaishan Hospital Yantai 264001 China.
Abstract:
Chemotherapy is one of the main treatment approaches for lung cancer. However, few drugs can be used in the post-first-line treatment of lung cancer. Apatinib is a small molecule inhibitor of vascular endothelial growth factor receptor-2 (VEGFR-2) and is widely used in advanced gastric cancer. This study aimed to investigate the therapeutic effect of apatinib in the second-line treatment of lung cancer and explore its underlying mechanism from the aspect of macrophage-mediated epithelial-mesenchymal transition (EMT). The results showed that apatinib attenuated macrophage-induced EMT and migration of lung cancer cells but not normal lung cells, as demonstrated by the loss of epithelial properties and gain of mesenchymal characteristics. Moreover, apatinib selectively decreased hepatocyte growth factor (HGF) secretion in polarized macrophages. Furthermore, apatinib down-regulated the expression of the HGF-Met signaling pathway in polarized macrophage-stimulated lung cancer cells. Taken together, our study has identified a novel pathway through which apatinib exerts its anti-cancer functions, and provided a molecular basis for apatinib potential applications in the post-first line treatment of lung cancer.
Insights
Apatinib, a VEGFR-2 inhibitor, shows promise in treating lung cancer by blocking macrophage-driven cell changes and migration. This offers a new option for post-first-line lung cancer therapy.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Therapeutics
Background:
- Lung cancer treatment options are limited after initial chemotherapy.
- Apatinib, a vascular endothelial growth factor receptor-2 (VEGFR-2) inhibitor, is approved for advanced gastric cancer.
- Investigating apatinib's efficacy and mechanism in second-line lung cancer treatment is crucial.
Purpose of the Study:
- To evaluate apatinib's therapeutic effect in second-line lung cancer treatment.
- To explore apatinib's mechanism involving macrophage-mediated epithelial-mesenchymal transition (EMT).
- To determine if apatinib impacts lung cancer cell migration and invasion.
Main Methods:
- Assessing apatinib's effect on macrophage-induced EMT in lung cancer cells.
- Measuring changes in epithelial and mesenchymal markers.
- Quantifying hepatocyte growth factor (HGF) secretion by polarized macrophages.
- Analyzing the HGF-Met signaling pathway in lung cancer cells.
Main Results:
- Apatinib inhibited macrophage-induced EMT and migration in lung cancer cells, not normal cells.
- Apatinib selectively reduced HGF secretion from polarized macrophages.
- Apatinib downregulated the HGF-Met signaling pathway in stimulated lung cancer cells.
Conclusions:
- Apatinib demonstrates anti-cancer effects by targeting macrophage-induced EMT and HGF-Met signaling.
- This study provides a molecular basis for apatinib's potential use in second-line lung cancer treatment.
- Apatinib represents a promising therapeutic strategy for advanced lung cancer.
