Amentoflavone Induces Cell-cycle Arrest, Apoptosis, and Invasion Inhibition in Non-small Cell Lung Cancer Cells

WEI-TING CHEN; CHENG-HSIEN CHEN; HUNG-TAI SU; PO-FU YUEH; FEI-TING HSU; I-TSANG CHIANG

doi:10.21873/anticanres.14893

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-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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Footnotes

↵* These Authors contributed equally to this study.
Authors’ Contributions
Data curation, WT Chen, CH Chen, HT Su, PF Yueh, FT Hsu and IT Chiang; funding acquisition, WT Chen, CH Chen and HT Su; writing – original draft, FT Hsu and IT Chiang; writing – review, IT Chiang. All Authors have read and agreed to the published version of the manuscript.
Conflicts of Interest
The Authors declare no conflicts of interest with the contents of this article.
Funding
This study was supported by a Grant from the Zuoying Branch of Kaohsiung Armed Forces General Hospital, Kaohsiung, Taiwan (Grant ID: KAFGH-ZY-A-109020), Show Chwan Memorial Hospital, Changhua, Taiwan (Grant ID: SRD-108007) and Taichung Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Taichung, Taiwan (Grant ID: TTCRD109-14), respectively. This work was also financially supported by the “Drug Development Center, China Medical University” from The Featured Areas Research Center Program within the framework of the Higher Education Sprout Project by the Ministry of Education (MOE) in Taiwan.

Received January 11, 2021.
Revision received January 21, 2021.
Accepted January 22, 2021.

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