Paris saponin II-induced paraptosis-associated cell death increased the sensitivity of cisplatin.

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.

• Authors: Shuli Man, Panpan Lv, Jingxia Cui, Furui Liu, Lei Peng, Long Ma, Changxiao Liu, Wenyuan Gao
• Journal: Toxicology and applied pharmacology (Toxicol Appl Pharmacol) Vol. 406 Pg. 115206 (11 01 2020) ISSN: 1096-0333 [Electronic] United States
• PMID: 32835762 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2020 Elsevier Inc. All rights reserved.

Chemical References

• Antineoplastic Agents
• Saponins
• formosanin C
• Diosgenin
• Cisplatin

Topics

• Antineoplastic Agents (pharmacology)
• Autophagy (drug effects)
• Cell Death (drug effects)
• Cell Line, Tumor
• Cisplatin (pharmacology)
• Diosgenin (analogs & derivatives, pharmacology)
• Endoplasmic Reticulum Stress (drug effects)
• Humans
• MAP Kinase Signaling System (drug effects)
• Saponins (pharmacology)