Shiau Jun-Ping, Chuang Ya-Ting, Tang Jen-Yang, Chen Shu-Rong, Hou Ming-Feng, Jeng Jiiang-Huei, Cheng Yuan-Bin, Chang Hsueh-Wei
Division of Breast Oncology and Surgery, Department of Surgery, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 80708, Taiwan.
Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan.
Antioxidants (Basel). 2022 Oct 4;11(10):1982. doi: 10.3390/antiox11101982.
The purpose of this study aimed to assess the antiproliferation effects of methanol extract of (METS) and explore the detailed responses of oral cancer cells compared to normal cells. METS effectively inhibits the cell proliferation of oral cancer cells but does not affect normal cell viability, exhibiting preferential antiproliferation function. METS exerted more subG1 accumulation, apoptosis induction, cellular and mitochondrial oxidative stress, and DNA damage than normal cells, reverted by oxidative stress inhibitor -acetylcysteine. This METS-caused oxidative stress was validated to attribute to the downregulation of glutathione. METS activated both extrinsic and intrinsic caspases. DNA double-strand breaks (γH2AX) and oxidative DNA damage (8-hydroxy-2-deoxyguanosine) were stimulated by METS. Therefore, for the first time, this investigation shed light on exploring the functions and responses of preferential antiproliferation of METS in oral cancer cells.
本研究旨在评估[具体植物名称]甲醇提取物(METS)的抗增殖作用,并探究口腔癌细胞与正常细胞相比的详细反应。METS可有效抑制口腔癌细胞的细胞增殖,但不影响正常细胞活力,表现出优先抗增殖功能。与正常细胞相比,METS导致更多的亚G1期积累、凋亡诱导、细胞和线粒体氧化应激以及DNA损伤,氧化应激抑制剂N-乙酰半胱氨酸可使其恢复。经证实,这种由METS引起的氧化应激归因于谷胱甘肽的下调。METS激活了外源性和内源性半胱天冬酶。METS刺激了DNA双链断裂(γH2AX)和氧化性DNA损伤(8-羟基-2-脱氧鸟苷)。因此,本研究首次揭示了METS在口腔癌细胞中优先抗增殖的功能和反应。