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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 저널정보
- 대한약리학회 The Korean Journal of Physiology & Pharmacology The Korean Journal of Physiology & Pharmacology 제24권 제6호
- 발행연도
- 2020.1
- 수록면
- 493 - 502 (10page)
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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?m), and ATP depletion, resulting in apoptosis and necroptosis in monolayer cell culture. Apigenin upregulated DNA damage response proteins, including the DNA double strand break marker phospho (p)- histone H2A.X. and caused a transition delay at the G2/M phase of cell cycle. Western blot analysis showed that apigenin treatment upregulated protein levels of cleaved caspase-3, cleaved PARP, p-MLKL, and p-RIP3 along with an increased Bax/Bcl-2 ratio. ATP supplementation restored cell viability and levels of DNA damage-, apoptosisand necroptosis-related proteins that apigenin caused. In addition, N-acetylcysteine reduced ROS production and improved Δ?m loss and cell death that were caused by apigenin. In a 3D spheroid culture model, ROS-dependent necroptosis was found to be a mechanism involved in the anti-cancer activity of apigenin against malignant mesothelioma cells. Taken together, our findings suggest that apigenin can induce ROS-dependent necroptotic cell death due to ATP depletion through mitochondrial dysfunction. This study provides us a possible mechanism underlying why apigenin could be used as a therapeutic candidate for treating malignant mesothelioma
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참고문헌 (27)
참고문헌 신청
Hartwell LH / 1989 / Checkpoints : controls that ensure the order of cell cycle events / Science 246:629~634
Zannini L / 2014 / CHK2 kinase in the DNA damage response and beyond / J Mol Cell Biol 6:442~457
Murphy MP / 2009 / How mitochondria produce reactive oxygen species / Biochem J 417:1~13
Higuchi Y / 2004 / Glutathione depletion-induced chromosomal DNA fragmentation associated with apoptosis and necrosis / J Cell Mol Med 8:455~464
Liu J / 2015 / Increased oxidative stress as a selective anticancer therapy / Oxid Med Cell Longev 2015:294303
Zannini L / 2014 / CHK2 kinase in the DNA damage response and beyond / J Mol Cell Biol 6:442~457
Murphy MP / 2009 / How mitochondria produce reactive oxygen species / Biochem J 417:1~13
Higuchi Y / 2004 / Glutathione depletion-induced chromosomal DNA fragmentation associated with apoptosis and necrosis / J Cell Mol Med 8:455~464
Liu J / 2015 / Increased oxidative stress as a selective anticancer therapy / Oxid Med Cell Longev 2015:294303
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