Amentoflavone Induces Cell-cycle Arrest, Apoptosis, and Invasion Inhibition in Non-small Cell Lung Cancer Cells
Autor: | I-Tsang Chiang, Cheng-Hsien Chen, Fei-Ting Hsu, Wei-Ting Chen, Po-Fu Yueh, Hung-Tai Su |
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Rok vydání: | 2021 |
Předmět: |
Vascular Endothelial Growth Factor A
Cancer Research Lung Neoplasms Cell cycle checkpoint Cytochrome P-450 CYP2C9 Inhibitors Cell Survival Apoptosis Amentoflavone Flow cytometry chemistry.chemical_compound Cell Movement Carcinoma Non-Small-Cell Lung Cell Line Tumor medicine Biflavonoids Humans Neoplasm Invasiveness Viability assay Reporter gene medicine.diagnostic_test Cell growth NF-kappa B Cell Cycle Checkpoints General Medicine G1 Phase Cell Cycle Checkpoints Matrix Metalloproteinases Vascular endothelial growth factor Oncology chemistry Cancer research Signal Transduction |
Zdroj: | Anticancer Research. 41:1357-1364 |
ISSN: | 1791-7530 0250-7005 |
DOI: | 10.21873/anticanres.14893 |
Popis: | Background/aim Amentoflavone, an effective compound derived from medicinal plants, has been shown to boost therapeutic efficacy of chemotherapy in non-small cell lung cancer (NSCLC). However, anti-NSCLC effect of amentoflavone is ambiguous. The major purpose of the present study was to verify the inhibitory effects of amentoflavone in NSCLC cells. Materials and methods The effects of amentoflavone on growth and invasion of NSCLC CL-1-5-F4 cells were evaluated by cell viability assay, flow cytometry, colony formation assay, nuclear factor-kappa B (NF-κB) reporter gene assay, immunofluorescence staining, transwell invasion, and western blot assay. Results Amentoflavone effectively induced cell growth inhibition, G1 cell-cycle arrest, apoptosis, and suppression of invasion. Furthermore, amentoflavone not only triggered expression of p27, cleaved caspase-3, -8 also reduced NF-κB signaling, protein levels of matrix metalloproteinase (MMP)-2, -9, Cyclin-D1, and vascular endothelial growth factor (VEGF). Conclusion Cell-cycle arrest, apoptosis induction, NF-κB signaling inhibition are associated with amentoflavone-inhibited growth and invasion of NSCLC cells. |
Databáze: | OpenAIRE |
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