王世盛

个人信息Personal Information

副教授

硕士生导师

性别:男

毕业院校:中科院大连化学物理研究所

学位:博士

所在单位:化工学院

学科:药物化学. 药物工程

办公地点:大连理工大学西部校区

联系方式:Office telephone:84986200

电子邮箱:wangss@dlut.edu.cn

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Induction of autophagy by an oleanolic acid derivative, SZC017, promotes ROS-dependent apoptosis through Akt and JAK2/STAT3 signaling pathway in human lung cancer cells

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论文类型:期刊论文

发表时间:2017-12-01

发表刊物:CELL BIOLOGY INTERNATIONAL

收录刊物:SCIE、PubMed

卷号:41

期号:12

页面范围:1367-1378

ISSN号:1065-6995

关键字:apoptosis; autophagy; JAK2; STAT3 signaling; lung cancer cells; SZC017

摘要:The signal transducers and activators of transcription 3 (STAT3) signaling pathway is a common feature in many solid tumors including non-small cell lung cancer, whereas current therapies usually fail to treat this disease in majority of cases. In the present study, we aimed to investigate the cytotoxic effect and the underlying mechanisms of SZC017, an oleanolic acid derivative, on human lung cancer cells. Cell viability was significantly decreased in SZC017-treated lung cancer cells. Mechanistically, SZC017 reduced A549 cell viability by activating both apoptosis and autophagy pathways. SZC017 was able to inhibit the phosphorylation of Akt, JAK2, and STAT3 in A549 cells, resulting in the inactivation of Akt and JAK2/STAT3 signaling pathways. In addition, SZC017 could induce ROS generation and Ca2+ release. Pretreatment with N-Acetyl L-Cysteine, a ROS scavenger, could fully reverse SZC017-induced ROS and increase the expression of Akt, p-STAT3, and procaspase-3, while decrease the ratio of LC3-II/I and the expression of Beclin-1. In summary, our study provides pharmacological evidence that SZC017 exhibits potential use in the treatment of lung cancer.