UM  > 中華醫藥研究院
Downregulation of Cyclin B1 mediates nagilactone E-induced G2 phase cell cycle arrest in non-small cell lung cancer cells
Zhang, Le-Le1; Feng, Zhe-Ling1; Su, Min-Xia1; Jiang, Xiao-Ming1; Chen, Xiuping1; Wang, Yitao1; Li, Ao2; Lin, Li-Gen1; Lu, Jin-Jian1
2018-07-05
Source PublicationEUROPEAN JOURNAL OF PHARMACOLOGY
ISSN0014-2999
Volume830Pages:17-25
Abstract

Non-small cell lung cancer (NSCLC) is one of the most common forms and leading causes of cancer-related mortality worldwide, and discovery of new effective drugs still remains imperative to improve the survival rate. Nagilactone E (NLE) is a natural product isolated from Podocarpus nagi seeds, which has been used as raw materials for edible oil and industrial oil extraction. This study aimed to investigate the anticancer potential of NLE against NSCLC A549 and NCI-H1975 cells. MTT assay revealed that NLE inhibited the proliferation of A549 and NCI-H1975 cells with IC(50)s of 5.18 +/- 0.49 and 3.57 +/- 0.29 mu M, respectively. NLE treatment inhibited clone formation in both cancer cell lines. Cell cycle analysis indicated that NLE treatment effectively induced G2 phase cell cycle arrest in A549 and NCI-H1975 cells. NLE downregulated the phosphorylation of cdc2 (Tyr15) and cdc25C (Ser216) as well as the expression level of the protein kinase Weel in concentration- and time-dependent manners. In addition, NLE treatment decreased the protein level of Cyclin B1 as well as its nuclear localization, which might decrease the activity of the Cyclin B1 /cdc2 complex and induce G2 phase arrest. Long-term NLE treatment also induced caspase-dependent cell apoptosis, as evidenced by increase in Annexin V positive cells and the cleavage of PARP. To sum, NLE inhibited proliferation, induced G2 phase arrest, and triggered caspase-dependent apoptosis in NSCLC cells, suggesting it to be a potential leading compound for cancer treatment.

KeywordNagilactone e Non-small Cell Lung Cancer Cyclin B1 Cell Cycle Apoptosis
DOIhttp://doi.org/10.1016/j.ejphar.2018.04.020
URLView the original
Indexed BySCI
Language英语
WOS Research AreaPharmacology & Pharmacy
WOS SubjectPharmacology & Pharmacy
WOS IDWOS:000432890900003
PublisherELSEVIER SCIENCE BV
The Source to ArticleWOS
Fulltext Access
Citation statistics
Document TypeJournal article
CollectionInstitute of Chinese Medical Sciences
Corresponding AuthorLin, Li-Gen
Affiliation1.State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China
2.College of Pharmacy and Bioengineering, Chongqing University of Technology, Chongqing, China
First Author AffilicationInstitute of Chinese Medical Sciences
Corresponding Author AffilicationInstitute of Chinese Medical Sciences
Recommended Citation
GB/T 7714
Zhang, Le-Le,Feng, Zhe-Ling,Su, Min-Xia,et al. Downregulation of Cyclin B1 mediates nagilactone E-induced G2 phase cell cycle arrest in non-small cell lung cancer cells[J]. EUROPEAN JOURNAL OF PHARMACOLOGY,2018,830:17-25.
APA Zhang, Le-Le.,Feng, Zhe-Ling.,Su, Min-Xia.,Jiang, Xiao-Ming.,Chen, Xiuping.,...&Lu, Jin-Jian.(2018).Downregulation of Cyclin B1 mediates nagilactone E-induced G2 phase cell cycle arrest in non-small cell lung cancer cells.EUROPEAN JOURNAL OF PHARMACOLOGY,830,17-25.
MLA Zhang, Le-Le,et al."Downregulation of Cyclin B1 mediates nagilactone E-induced G2 phase cell cycle arrest in non-small cell lung cancer cells".EUROPEAN JOURNAL OF PHARMACOLOGY 830(2018):17-25.
Related Services
Recommend this item
Bookmark
Usage statistics
Export to Endnote
Google Scholar
Similar articles in Google Scholar
[Zhang, Le-Le]'s Articles
[Feng, Zhe-Ling]'s Articles
[Su, Min-Xia]'s Articles
Baidu academic
Similar articles in Baidu academic
[Zhang, Le-Le]'s Articles
[Feng, Zhe-Ling]'s Articles
[Su, Min-Xia]'s Articles
Bing Scholar
Similar articles in Bing Scholar
[Zhang, Le-Le]'s Articles
[Feng, Zhe-Ling]'s Articles
[Su, Min-Xia]'s Articles
Terms of Use
No data!
Social Bookmark/Share
File name: Zhang-2018-Downregulation-of-cyclin-b-mediates.pdf
Format: Adobe PDF
All comments (0)
No comment.
 

Items in the repository are protected by copyright, with all rights reserved, unless otherwise indicated.