巴黎七叶皂苷 II 诱导的 paraptosis 相关细胞死亡增加了顺铂的敏感性。
Paris saponin II-induced paraptosis-associated cell death increased the sensitivity of cisplatin.
机构信息
State Key Laboratory of Food Nutrition and Safety, Key Laboratory of Industrial Microbiology, Ministry of Education, Tianjin Key Laboratory of Industry Microbiology, National and Local United Engineering Lab of Metabolic Control Fermentation Technology, National and Local United Engineering Lab of Metabolic Control Fermentation Technology, China International Science and Technology Cooperation Base of Food Nutrition/Safety and Medicinal Chemistry, College of Biotechnology, Tianjin University of Science & Technology, Tianjin 300457, China.
State Key Laboratory of Food Nutrition and Safety, Key Laboratory of Industrial Microbiology, Ministry of Education, Tianjin Key Laboratory of Industry Microbiology, National and Local United Engineering Lab of Metabolic Control Fermentation Technology, National and Local United Engineering Lab of Metabolic Control Fermentation Technology, China International Science and Technology Cooperation Base of Food Nutrition/Safety and Medicinal Chemistry, College of Biotechnology, Tianjin University of Science & Technology, Tianjin 300457, China.
出版信息
Toxicol Appl Pharmacol. 2020 Nov 1;406:115206. doi: 10.1016/j.taap.2020.115206. Epub 2020 Aug 21.
Paris Saponin II (PSII) has been regarded as an effective and imperative component isolated from Rhizoma Paridis saponins (RPS) and exhibited strong anti-tumor effects on a variety of cancer. Our results revealed that human non-small lung cancer cell lines NCI-H460 and NCI-H520 were exposed to 1 μM of PSII, which inhibited the proliferation of lung cancer cells and activated apoptosis, autophagy and paraptosis. PSII induced paraptosis-associated cell death prior to apoptosis and autophagy. It induced paraptosis based on ER stress through activation of the JNK pathway. Meanwhile, PSII increased the cytotoxicity of cisplatin through paraptosis-associated pathway. All in all, PSII induced paraptosis based on induction of non-apoptotic cell death, which would be a possible approach to suppress the multi-drug resistant to apoptosis.
巴黎七叶皂甙 II（PSII）已被视为从重楼皂苷（RPS）中分离出来的一种有效且必需的成分，对多种癌症具有强烈的抗肿瘤作用。我们的研究结果表明，人非小细胞肺癌细胞系 NCI-H460 和 NCI-H520 暴露于 1 μM 的 PSII 后，抑制了肺癌细胞的增殖并激活了细胞凋亡、自噬和副凋亡。PSII 在细胞凋亡和自噬之前诱导副凋亡相关的细胞死亡。它通过激活 JNK 通路，基于内质网应激诱导副凋亡。同时，PSII 通过副凋亡相关途径增加顺铂的细胞毒性。总之，PSII 通过诱导非凋亡性细胞死亡诱导副凋亡，这可能是抑制多药耐药性细胞凋亡的一种方法。
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