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ORIGINAL ARTICLE
Year : 2022  |  Volume : 65  |  Issue : 3  |  Page : 136-142

A synthetic biscoumarin suppresses lung cancer cell proliferation and induces cell apoptosis by increasing expression of RIP1


1 School of Medicine, Foshan University, Foshan, Guangdong, China
2 Guangdong Engineering Research Center of Natural Products and New Drugs, Guangdong Provincial University Engineering Technology Research Center of Natural Products and Drugs, Guangdong Pharmaceutical University, Guangzhou, China
3 School of Medicine, Foshan University; R&D Department, Foshan Newtopcome Pharmaceutical Technology Co., Ltd., Foshan, Guangdong, China

Correspondence Address:
Dr. Zhaoguang Zheng
School of Medicine, Foshan University, 5 Hebin Road, Chancheng Area, Foshan; R&D Department, Foshan Newtopcome Pharmaceutical Technology Co., Ltd., No. 129 West Jihua Road, Chancheng Area, Foshan, Guangdong
China
Prof. Zhengquan Su
Guangdong Engineering Research Center of Natural Products and New Drugs, Guangdong Provincial University Engineering Technology Research Center of Natural Products and Drugs, Guangdong Pharmaceutical University, 280 Waihuan East Road, Guangzhou
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/cjp.cjp_107_21

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Coumarin has a variety of biological activities and widely exists in plants. Biscoumarin, derived from coumarin, their synthetic methods and bioactivities of biscoumarins is the hotspot of the current research. In this study, we evaluated for the first time the anticancer of a synthetic biscoumarin (3,3'-(4-chlorophenyl)methylene)bis(4-hydroxy-2H-chromen-2-one, C3) on lung cancer cells and explored the related mechanism. C3 was simply prepared by 4-hydroxycoumarin and 4-chlorobenzaldehyde under ethanol. The structure of C3 was elucidated by various spectroscopic analyses. The antiproliferation effect of C3 was evaluated by the cell counting kit-8 assay. Cell cycle and apoptosis analysis were detected by flow cytometry. The expression of correlated proteins was determined using Western blotting. The result showed that C3 displayed a strong cytostatic effect on Lewis lung cancer (LLC) cells. C3 inhibited the proliferation of LLC cells, and induced G2/M phase cell cycle arrest. In addition, C3 possessed a significant reduction on cell apoptosis by increasing of RIP1 expression. Our data showed that C3 suppresses lung cancer cell proliferation and induces cell apoptosis, which is possibly involved with the RIP1.


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