ArticleExperimental and therapeutic medicine2020
Dexamethasone and lenvatinib inhibit migration and invasion of non-small cell lung cancer by regulating EKR/AKT and VEGF signal pathways.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- Blood-based detection of lung cancer using cysteine-rich angiogenic inducer 61 (CYR61) as a circulating protein biomarker: a pilot study.Molecular oncology · 2021Trial
- Dexamethasone drives macrophage repolarization linked to increased triple-negative breast cancer aggressiveness.Cell death & disease · 2025Article
- Dexamethasone improves thymoma-associated myasthenia gravis via the AKT-mTOR pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Combination of Vitamin C and Lenvatinib potentiates antitumor effects in hepatocellular carcinoma cellsPeerJ · 2023Article
- Drug repositioning in non-small cell lung cancer (NSCLC) using gene co-expression and drug-gene interaction networks analysis.Scientific reports · 2022Article
- AIF-1, a potential biomarker of aggressive tumor behavior in patients with non-small cell lung cancer.PloS one · 2022Article
- Article
- Ropivacaine Inhibits Lung Cancer Cell Malignancy Through Downregulation of Cellular Signaling Including HIF-1αFrontiers in pharmacology · 2021Article
- The Roles of CCN1/CYR61 in Pulmonary Diseases.International journal of molecular sciences · 2020Review
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Authors and funding
5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Migration and invasion is one of the most important features in tumor metastasis and development. Non-small cell lung cancer (NSCLC) is one of the most common types of cancer globally, and has been linked to air contamination. Evidence indicates that cysteine-rich angiogenic inducer 61 (CYR61) is associated with the migration and invasion of NSCLC. Overexpression of CYR61 protein promotes the migration and the transition of tumor-derived vascular endothelial cells in NSCLC. However, the association between CYR61 and NSCLC remains poorly understood. Lenvatinib is an oral multi-target drug that targets various receptors upon tumor angiogenesis. Dexamethasone is widely approved for combination therapy in patients with NSCLC. In the current study, the expression and function of CYR61 in NSCLC was analyzed during the progression of NSCLC. Inhibitory effects on migration and invasion induced by lenvatinib and dexamethasone were determined by migratory and invasion assays. Migratory pathways of extracellular signal-regulated kinases (ERK) and protein kinase B (AKT) were also investigated by targeting vascular endothelial growth factor (VEGF) and CYR61 via synergistic treatment with transforming growth factor-β1 (TGF-β1) and dexamethasone. Therapeutic outcomes of combined treatment with lenvatinib and dexamethasone were assessed in NSCLC-bearing mice. The results of the present study indicate that cooperative treatment of lenvatinib and dexamethasone significantly inhibited TGF-β1-induced cell migration and suppressed tumor growth (P<0.01). Notably, the results demonstrated that dexamethasone eradicated the promotion effects of TGF-β1 on the AKT/epithelial-mesenchymal transition process and lenvatinib extinguished tumor cell metastasis by targeting VEGF. The results of the current study also demonstrate that dexamethasone suppressed the expression of CAG-I and enhanced expression of matrix metalloproteinase-1. Synergistic treatment for NSCLC was demonstrated to be efficacious. In conclusion, dexamethasone inhibited AKT/ERK phosphorylation and lenvatinib antagonism bound VEGF leading to the limitation of migration and invasion of cancer cells in NSCLC.
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