| Literature DB >> 32835762 |
Shuli Man1, Panpan Lv2, Jingxia Cui2, Furui Liu2, Lei Peng2, Long Ma2, Changxiao Liu3, Wenyuan Gao4.
Abstract
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.Entities:
Keywords: Cytoplasmic Vacuolation; Endoplasmic Reticulum Stress; Mitochondrial Swelling; Paraptosis; Paris Saponin II
Year: 2020 PMID: 32835762 DOI: 10.1016/j.taap.2020.115206
Source DB: PubMed Journal: Toxicol Appl Pharmacol ISSN: 0041-008X Impact factor: 4.219