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Impacts of combination of Paris Saponins Ⅱ and camptothecin on apoptosis and signal pathways in lung cancer H460, H446 cells
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DOI   10.11656/j.issn.1672-1519.2019.02.19
Key Words   Paris Saponins Ⅱ;lung cancer;camptothecin;combination drugs
Author NameAffiliationE-mail
GUO Huimin Tianjin Technology Property Rights Exchange Co., Ltd, Tianjin 300203, China  
LI Yiliang Institute of Radiation Medicine, Chinese Academy of Medical Science and PekingUnion Medical College, Tianjin 300192, China liyiliang75@163.com 
LIU Zhen China International Science and Technology Cooperation Base of Food Nutrition/Safety and Medicinal Chemistry, Key Laboratory of Industrial Fermentation Microbiology of Ministry of Education, Tianjin Key Laboratory of Industry Microbiology, College of Biotechnology, Tianjin University of Science & Technology, Tianjin 300457, China liuzhen5957@163.com 
Abstract
    [Objective] To investigate the effects and mechanism of Pariss saponins (PSⅡ) combined with Camptothecin (CPT) on lung cancer cell line.[Methods] The effects of PSⅡ combined with CPT on the proliferation activity on non-small cell lung cancer H460 cells and small cell lung cancer H446 cells were deteceted by MTT. Cloning plating efficiency of PSⅡ combined with CPT was studied by flat plate clone formation test. Cell apoptosis was analyzed by flow cytometry. Phosphorylation acitivities (AKT, ERK and p38 MAPK) and expression levels of anti-apoptosis protein and Bcl-2 and Bcl-XL were analyzed by Western Blot.[Results] MTT assay showed that PSⅡ combined with CPT had a cytotoxic effect on lung cancer cell in a dose-dependent manner. Strong synergism of PSⅡ combined with CPT was observed in cell clone formation assay. The late apoptosis rate was increased when PSⅡ combined with CPT, and the early apoptosis rate of H446 was significantly increased to (70.10±3.44)%. Western blot result showed that the expression of p38 MAPK and ERK phosphorylation were significantly increased when using PSⅡ combined with CPT on H460, however, there was no obvious effect on the expression of AKT; and the expression of Bcl-2 and Bcl-XL were reduced. PSⅡ combined with CPT can increased the expression of AKT, p38 MAPK and ERK phosphorylation and decreased the expression of Bcl-2 of H446, there was no obvious effect on the expression of Bcl-XL.[Conclusion] PSⅡ exhibits cytotoxicity in different pathways in lung cancer cells and it can be used as a chemosensitizer to CPT in lung cancer cells.

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