Amentoflavone induces cell-cycle arrest, apoptosis, and invasion inhibition in non-small cell lung cancer cells

Abstract

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-ĸB) 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-ĸB signaling, protein levels of matrix metalloproteinase (MMP)-2, -9, Cyclin-D1, and vascular endothelial growth factor (VEGF). Conclusion: Cell-cycle arrest, apoptosis induction, NF-ĸB signaling inhibition are associated with amentoflavone-inhibited growth and invasion of NSCLC cells.