Amentoflavone Induces Cell-cycle Arrest, Apoptosis, and Invasion Inhibition in Non-small Cell Lung Cancer Cells
- Anticancer Res. 2021 Mar;41(3):1357-1364. doi: 10.21873/anticanres.14893.
- 1. Department of Psychiatry, Zuoying Branch of Kaohsiung Armed Forces General Hospital, Kaohsiung, Taiwan, R.O.C.
- 2. Surgical department of Show Chwan Memorial Hospital, Changhua, Taiwan, R.O.C.
- 3. Division of Anesthesiology, Taichung Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Taichung, Taiwan, R.O.C.
- 4. School of Medicine, Tzu Chi University, Hualien, Taiwan, R.O.C.
- 5. Institute of Traditional Medicine, School of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan, R.O.C.
- 6. Department of Biological Science and Technology, China Medical University, Taichung, Taiwan, R.O.C.
- 7. Department of Radiation Oncology, Show Chwan Memorial Hospital, Changhua, Taiwan, R.O.C.; [email protected].
- 8. Department of Radiation Oncology, Chang Bing Show Chwan Memorial Hospital, Changhua, Taiwan, R.O.C.
- 9. Department of Medical Imaging and Radiological Sciences, Central Taiwan University of Science and Technology, Taichung, Taiwan, R.O.C.
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.
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