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Original Article

Korean J Physiol Pharmacol 2020; 24(6): 493-502

Published online November 1, 2020 https://doi.org/10.4196/kjpp.2020.24.6.493

Copyright © Korean J Physiol Pharmacol.

Apigenin causes necroptosis by inducing ROS accumulation, mitochondrial dysfunction, and ATP depletion in malignant mesothelioma cells

Yoon-Jin Lee1, Kwan-Sik Park1, Hae-Seon Nam2, Moon-Kyun Cho2, and Sang-Han Lee1,*

1Department of Biochemistry, Soonchunhyang University College of Medicine, 2Division of Molecular Cancer Research, Soonchunhyang Medical Research Institute, Soonchunhyang University, Cheonan 31151, Korea

Correspondence to:Sang-Han Lee
E-mail: m1037624@sch.ac.kr

Received: June 17, 2020; Revised: September 12, 2020; Accepted: September 26, 2020

This is an Open Access journal distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Apigenin, a naturally occurring flavonoid, is known to exhibit significant anticancer activity. This study was designed to determine the effects of apigenin on two malignant mesothelioma cell lines, MSTO-211H and H2452, and to explore the underlying mechanism(s). Apigenin significantly inhibited cell viability with a concomitant increase in intracellular reactive oxygen species (ROS) and caused the loss of mitochondrial membrane potential (Δ

Keywords: Apigenin, Apoptosis, Mesothelioma, Necroptosis, Reactive oxygen species