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7-Methoxy-1-Tetralone Induces Apoptosis, Suppresses Cell Proliferation and Migration in Hepatocellular Carcinoma via Regulating c-Met, p-AKT, NF-κB, MMP2, and MMP9 Expression.
Frontiers in Oncology ( IF 3.5 ) Pub Date : 2020-02-07 , DOI: 10.3389/fonc.2020.00058
Ying Wen 1, 2 , Xiaoyan Cai 2 , Shaolian Chen 3 , Wei Fu 1, 2 , Dong Chai 1, 2 , Huainian Zhang 1, 2 , Yongli Zhang 1, 2
Affiliation  

This study aimed to determine the anti-proliferative and anti-migratory effects of 7-methoxy-1-tetralone (MT) in hepatocellular carcinoma (HCC) cells. MTT assay assessed HCC cell viability; cell apoptosis of HCC cells was determined by flow cytometry; wound healing assay evaluated HCC cell migratory ability; protein expression levels were assessed using western blot assay; the in vivo antitumor effects of MT were tested in BALB/c nude mice and the pathological changes within the tumor tissues were evaluated by immunohistochemistry. MT treatment significantly suppressed the cell proliferative and migratory potentials of HepG2 cells, and induced HepG2 cell apoptosis. The western blot assay showed that MT treatment caused a suppression on c-Met, phosphorylated AKT (p-AKT), NF-κB, matrix metallopeptidase 2 (MMP2)/MMP9 protein levels in HepG2 cells. Further in vivo animal studies deciphered that MT treatment suppressed tumor growth of HepG2 cells in the nude mice, but had no effect on the body weight and the organ index of liver and spleen. Further immunohistochemistry analysis of the dissected tumor tissues showed that MT treatment significantly suppressed the protein expression levels of NF-κB, MMP9, MMP2, and p-AKT. In summary, the present study demonstrated the anti-tumor effects of MT on the HCC, and MT suppressed HCC progression possibly via regulating proliferation- and migration-related mediators including c-Met, p-AKT, NF-κB, MMP2, and MMP9 in HepG2 cells.

中文翻译:

7-甲氧基-1-四氢萘酮可通过调节c-Met,p-AKT,NF-κB,MMP2和MMP9表达诱导肝癌细胞凋亡,抑制细胞增殖和迁移。

这项研究旨在确定7-甲氧基-1-四氢萘酮(MT)在肝细胞癌(HCC)细胞中的抗增殖和抗迁移作用。MTT法评估肝细胞的生存能力;流式细胞仪检测肝癌细胞的凋亡。伤口愈合试验评估了HCC细胞迁移能力;使用蛋白质印迹分析评估蛋白质表达水平;在BALB / c裸鼠中测试MT的体内抗肿瘤作用,并通过免疫组织化学评估肿瘤组织内的病理变化。MT治疗显着抑制HepG2细胞的增殖和迁移潜能,并诱导HepG2细胞凋亡。Western blot分析表明,MT处理可抑制HepG2细胞中c-Met,磷酸化AKT(p-AKT),NF-κB,基质金属肽酶2(MMP2)/ MMP9蛋白水平。进一步的体内动物研究认为,MT处理可抑制裸鼠中HepG2细胞的肿瘤生长,但对体重以及肝和脾脏器官指数没有影响。对解剖的肿瘤组织的进一步免疫组织化学分析表明,MT处理显着抑制了NF-κB,MMP9,MMP2和p-AKT的蛋白表达水平。总之,本研究证明了MT对HCC的抗肿瘤作用,并且MT可能通过调节与增殖和迁移相关的介质(包括c-Met,p-AKT,NF-κB,MMP2和MMP9)抑制了HCC进程。在HepG2细胞中 对解剖的肿瘤组织的进一步免疫组织化学分析表明,MT处理显着抑制了NF-κB,MMP9,MMP2和p-AKT的蛋白表达水平。总之,本研究证明了MT对HCC的抗肿瘤作用,并且MT可能通过调节与增殖和迁移相关的介质(包括c-Met,p-AKT,NF-κB,MMP2和MMP9)抑制了HCC进程。在HepG2细胞中 对解剖的肿瘤组织的进一步免疫组织化学分析表明,MT处理显着抑制了NF-κB,MMP9,MMP2和p-AKT的蛋白表达水平。总而言之,本研究证明了MT对HCC的抗肿瘤作用,并且MT可能通过调节与增殖和迁移相关的介质(包括c-Met,p-AKT,NF-κB,MMP2和MMP9)抑制了HCC进程。在HepG2细胞中
更新日期:2020-02-07
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