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Retracted : Sapylin inhibits lung cancer cell proliferation and promotes apoptosis by attenuating PI3K/AKT signaling
Author(s) -
Zhang Lin,
Liu Benhong
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28729
Subject(s) - pi3k/akt/mtor pathway , protein kinase b , apoptosis , cell growth , viability assay , a549 cell , microbiology and biotechnology , cancer research , chemistry , signal transduction , biology , biochemistry
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.