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撤稿文章：氧杂蒽酮衍生物的合成及抗肝细胞癌效力评估：诱导凋亡

Retracted Article: Synthesis of xanthone derivatives and anti-hepatocellular carcinoma potency evaluation: induced apoptosis.

作者信息

Liu Jie, Bao Hui, Wang Huailing, Luo Qiang, Zuo Jianhong, Liu Zhigang, Qiu Shuqi, Sun Xizhuo, Liu Xiaoyu

机构信息

The Third Affiliated Hospital of ShenZhen University Shenzhen 518020 China

School of Medicine, Shenzhen University Shenzhen 518060 China

出版信息

RSC Adv. 2019 Dec 9;9(70):40781-40791. doi: 10.1039/c9ra06408g.

DOI:10.1039/c9ra06408g
PMID:35540078
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9076231/
Abstract

Twenty-one xanthone derivatives (XDs) were synthesized by a microwave-assisted technique. Their inhibition potency against the growth of four cancer cell lines was evaluated. XD-1 ∼ [6,9,10-trihydroxy-3,3-dimethyl-5-(2-methylbut-3-en-2-yl)-3,7-pyrano[2,3-]xanthen-7-one] was confirmed as the most active agent against HepG2 cell line growth with IC of 18.6 ± 2.31 μM. Apoptosis analysis indicated different contributions of early/late apoptosis and necrosis to cell death for XD-1. XD-1 arrested HepG2 cells on the G0/G1 phase, as indicated by the decreased expressions of cyclin D and CDK2 and the increased expressions of p21. Western blot implied that XD-1 regulated p53/MDM2 to a better healthier state. Moreover, XD-1-induced cell apoptosis was mitochondrion-mediated, as evidenced by caspase activation and involved the PI3K/AKT/mTOR signaling pathway. All the evidence supports that XD-1 is a significant anti-cancer agent for HCC.

摘要

通过微波辅助技术合成了21种氧杂蒽衍生物（XDs）。评估了它们对四种癌细胞系生长的抑制效力。XD-1 ∼ [6,9,10-三羟基-3,3-二甲基-5-(2-甲基丁-3-烯-2-基)-3,7-吡喃并[2,3-]氧杂蒽-7-酮]被确认为对HepG2细胞系生长最具活性的药物，其IC50为18.6 ± 2.31 μM。凋亡分析表明早期/晚期凋亡和坏死对XD-1诱导的细胞死亡有不同贡献。如细胞周期蛋白D和细胞周期蛋白依赖性激酶2（CDK2）表达降低以及p21表达增加所示，XD-1使HepG2细胞停滞在G0/G1期。蛋白质印迹法表明XD-1将p53/MDM2调节至更好的健康状态。此外，XD-1诱导的细胞凋亡是线粒体介导的，这通过半胱天冬酶激活得到证实，并且涉及PI3K/AKT/mTOR信号通路。所有证据均支持XD-1是一种用于肝癌的重要抗癌药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d4e/9076231/44ce13d543d6/c9ra06408g-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d4e/9076231/712500a7932d/c9ra06408g-s1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d4e/9076231/cf0a8cc67d0b/c9ra06408g-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d4e/9076231/c41d82327d8e/c9ra06408g-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d4e/9076231/04ab8aefd0a4/c9ra06408g-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d4e/9076231/44ce13d543d6/c9ra06408g-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d4e/9076231/712500a7932d/c9ra06408g-s1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d4e/9076231/cf0a8cc67d0b/c9ra06408g-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d4e/9076231/c41d82327d8e/c9ra06408g-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d4e/9076231/04ab8aefd0a4/c9ra06408g-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d4e/9076231/44ce13d543d6/c9ra06408g-f4.jpg

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