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Sapylin inhibits lung cancer cell proliferation and promotes apoptosis by attenuating PI3K/AKT signaling.

Authors
  • Zhang, Lin1
  • Liu, Benhong2
  • 1 Department of Health Materials Management, Dongying People's Hospital, Dongying, Shandong, China. , (China)
  • 2 Department of Respiratory Medicine, Dongying People's Hospital, Dongying, Shandong, China. , (China)
Type
Published Article
Journal
Journal of Cellular Biochemistry
Publisher
Wiley (John Wiley & Sons)
Publication Date
Sep 01, 2019
Volume
120
Issue
9
Pages
14679–14687
Identifiers
DOI: 10.1002/jcb.28729
PMID: 31009136
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Sapylin (OK-432) revealed biological properties in cancers. In this study, the effect of sapylin on lung cancer cell A549 was investigated. A549 cell lines were treated with sapylin (0.1, 0.5, and 1 KE/mL) for different time intervals. A549 cell proliferation and apoptosis was determined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide/Ki67 assay and flow cytometry, respectively. Western blot was used to determine the expressions of proteins involved in proliferation, apoptosis, and phosphoinositide 3-kinase/serine/threonine kinase (PI3K/AKT), Wnt3a/β-catenin signaling pathway. Level of intracellular reactive oxygen species (ROS) was insured by using the ROS kit. Sapylin inhibited A549 cell viability and the expressions of proliferation-related proteins (cyclin E1 and D1) in dose- and time-dependent manners. Sapylin promoted apoptosis in a dose- and time-dependent manners. Sapylin also promoted the expressions of apoptotic proteins (cleaved caspase-3 and 8) in dose- and time-dependent manners. Furthermore, sapylin increased the intracellular concentration of ROS in a dose-dependent manner. Besides, the high expression of ROS level might induce inhibition of cell viability and increase cell apoptosis. The mechanistic study revealed that sapylin inactivated the PI3K/AKT and Wnt3a/β-catenin signaling pathways. Our findings suggest that sapylin inhibits proliferation and promotes apoptosis in lung cancer cells, thus providing a new theoretical basis for the treatment of lung cancer. © 2019 Wiley Periodicals, Inc.

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