Propyl isothiocyanate induces apoptosis in gastric cancer cells by oxidative stress via glutathione depletion
Propyl isothiocyanate induces apoptosis in gastric cancer cells by oxidative stress via glutathione depletion
复制标题
异硫氰酸丙酯通过谷胱甘肽消耗导致氧化应激诱导胃癌细胞凋亡
DOI：
10.3892/ol.2019.10875
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发表时间：
2019-11-01
期刊：
影响因子：
2.9
通讯作者：
Gu, Jun
中科院分区：
文献类型：
--
作者：
Huang, Ling;Cai, Chen;Gu, Jun
异硫氰酸盐是大多数十字花科植物中存在的一组化合物。许多异硫氰酸酯已被证明具有抗癌作用；然而，异硫氰酸丙酯 (PITC) 的抗肿瘤特性此前尚未得到评估。在本研究中，研究了PITC对胃癌（GC）细胞的可能影响，并探讨了潜在的潜在机制。结果表明，PITC 抑制两种 GC 细胞系的细胞活力并诱导细胞周期停滞和凋亡。 PITC 治疗促进 GC 细胞系中谷胱甘肽的消耗，导致活性氧积累和 DNA 损伤，从而激活线粒体依赖性和 p53 信号通路，引发 GC 细胞凋亡。 N-乙酰-L-半胱氨酸可逆转 PITC 的作用。本研究的结果揭示了 PITC 诱导 GC 细胞凋亡的潜在机制，这可能是由线粒体依赖性细胞凋亡和 DNA 损伤介导的。
Isothiocyanates are a group of compounds that exist in the majority of cruciferous plants. A number of isothiocyanates have been demonstrated to exhibit anticancer effects; however, antitumor properties of propyl isothiocyanate (PITC) have not been evaluated previously. In this study, the possible effects of PITC on gastric cancer (GC) cells were investigated, and the potential underlying mechanisms were explored. The results demonstrated that PITC inhibited cell viability of two GC cell lines and induced cell cycle arrest and apoptosis. Treatment with PITC promoted total glutathione depletion in GC cell lines, leading to reactive oxygen species accumulation and DNA damage, which activated the mitochondria-dependent and p53 signaling pathways to trigger apoptosis in GC cells. The effects of PITC were reversed by N-Acetyl-L-cysteine. The results of the present study revealed the potential mechanisms of PITC on apoptosis induction in GC cells, which may be mediated by mitochondria-dependent apoptosis and DNA damage.