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Induction of reactive oxygen species-stimulated distinctive autophagy by chelerythrine in non-small cell lung cancer cells
Tang, Zheng-Hai1; Cao, Wen-Xiang1; Wang, Zhao-Yu1; Lu, Jia-Hong1; Liu, Bo2; Chen, Xiuping1; Lu, Jin-Jian1
2017-08
Source PublicationREDOX BIOLOGY
ISSN2213-2317
Volume12Pages:367-376
Abstract

Chelerythrine (CHE), a natural benzo[c] phenanthridine alkaloid, shows anti-cancer effect through a number of mechanisms. Herein, the effect and mechanism of the CHE-induced autophagy, a type II programmed cell death, in non-small cell lung cancer (NSCLC) cells were studied for the first time. CHE induced cell viability decrease, colony formation inhibition, and apoptosis in a concentration-dependent manner in NSCLC A549 and NCI-H1299 cells. In addition, CHE triggered the expression of phosphatidylethanolamine-modified microtubule-associated protein light-chain 3 (LC3-II). The CHE-induced expression of LC3-II was further increased in the combination treatment with chloroquine (CQ), an autophagy inhibitor, and large amounts of red-puncta were observed in the CHE-treated A549 cells with stable expression of mRFP-EGFP-LC3, indicating that CHE induces autophagy flux. Silence of beclin 1 reversed the CHE-induced expression of LC3-II. Inhibition of autophagy remarkably reversed the CHE-induced cell viability decrease and apoptosis in NCI-H1299 cells but not in A549 cells. Furthermore, CHE triggered reactive oxygen species (ROS) generation in both cell lines. A decreased level of ROS through pretreatment with N-acetyl-L-cysteine reversed the CHE-induced cell viability decrease, apoptosis, and autophagy. Taken together, CHE induced distinctive autophagy in A549 (accompanied autophagy) and NCI-H1299 (pro-death autophagy) cells and a decreased level of ROS reversed the effect of CHE in NSCLC cells in terms of cell viability, apoptosis, and autophagy.

KeywordChelerythrine Autophagy Apoptosis Ros Nsclc
DOI10.1016/j.redox.2017.03.009
URLView the original
Indexed BySCI
Language英语
WOS Research AreaBiochemistry & Molecular Biology
WOS SubjectBiochemistry & Molecular Biology
WOS IDWOS:000403328700034
PublisherELSEVIER SCIENCE BV
The Source to ArticleWOS
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被引频次[WOS]:17   [WOS记录]     [WOS相关记录]
Document TypeJournal article
专题Institute of Chinese Medical Sciences
Affiliation1.State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China
2.The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangdong Provincial Academy of Chinese Medical Sciences, Guangzhou, China
First Author AffilicationInstitute of Chinese Medical Sciences
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Tang, Zheng-Hai,Cao, Wen-Xiang,Wang, Zhao-Yu,et al. Induction of reactive oxygen species-stimulated distinctive autophagy by chelerythrine in non-small cell lung cancer cells[J]. REDOX BIOLOGY,2017,12:367-376.
APA Tang, Zheng-Hai.,Cao, Wen-Xiang.,Wang, Zhao-Yu.,Lu, Jia-Hong.,Liu, Bo.,...&Lu, Jin-Jian.(2017).Induction of reactive oxygen species-stimulated distinctive autophagy by chelerythrine in non-small cell lung cancer cells.REDOX BIOLOGY,12,367-376.
MLA Tang, Zheng-Hai,et al."Induction of reactive oxygen species-stimulated distinctive autophagy by chelerythrine in non-small cell lung cancer cells".REDOX BIOLOGY 12(2017):367-376.
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