Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Apigenin-7-glucoside induces apoptosis and ROS accumulation in lung cancer cells, and inhibits PI3K/Akt/mTOR pathway

Chen Chen, Sheng Zhong, Hua Wu, Jintong Ge, Qi Wang

Department of Thoracic Surgery, The Affiliated Huaiâ€™an No. 1 Peopleâ€™s Hospital of Nanjing Medical University, Huai'an City, Jiangsu Province 223000, China;

For correspondence:- Qi Wang Email: hayywq@njmu.edu.cn

Accepted: 4 May 2023 Published: 30 May 2023

Citation: Chen C, Zhong S, Wu H, Ge J, Wang Q. Apigenin-7-glucoside induces apoptosis and ROS accumulation in lung cancer cells, and inhibits PI3K/Akt/mTOR pathway. Trop J Pharm Res 2023; 22(5):937-943 doi: 10.4314/tjpr.v22i5.1

© 2023 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To investigate how apigenin-7-glucoside (AGL) affects the proliferation, migration, invasion, and reactive oxygen species (ROS) accumulation in lung cancer cells, and to evaluate the potential of AGL as a therapeutic target.

Methods: Human bronchial epithelial cells (BEAS-2B), human lung carcinoma (A549), and non-small cell lung cancer cells (H1975), were treated with 25, 50, 100, and 200 μM AGL. Cell viability curves and EdU assays were used to evaluate their proliferation, while apoptosis was assessed by flow cytometry. Cell migration and invasion were evaluated by Transwell assays, and western blot was performed to determine the expression level of cytochrome C and phosphorylation of PI3K, AKT, and mTOR. Furthermore, ELISA was used to quantify the level of malondialdehyde (MDA) and glutathione (GSH). Indirect immunofluorescent assay (IFA) was performed by staining with DCFH-DA to evaluate ROS level.

Results: Proliferation of A549 and H1975 cells was suppressed by AGL in a dose-dependent manner. AGL significantly reduced proliferation, promoted cell apoptosis, and attenuated the migration and invasion of A549 or H1975 cells. It also elevated the levels of cytochrome C and MDA but reduced the production of GSH in A549 and H1975 cells. AGL enhanced the accumulation of ROS and weakened phosphorylation of AKT, PI3K, and mTOR in A549 and H1975 cells.

Conclusion: AGL represses proliferation, promotes apoptosis, suppresses migration and invasion, and induces ROS accumulation in lung cancer cells by repressing PI3K/Akt/mTOR pathway, thus indicating the potential of AGL as a target in lung cancer treatment

Keywords: Apigenin-7-glucoside, Apoptosis, Lung cancer, Phosphorylation, Reactive oxygen species