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Tumoricidal activities of pterostilbene depend upon destabilizing the MTA1-NuRD complex and enhancing P53 acetylation in hepatocellular carcinoma

机译:蝶芪的杀肿瘤活性取决于稳定MTA1-NuRD复合物的稳定性并增强肝细胞癌的P53乙酰化

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摘要

The present study aimed to assess the tumoricidal effect of metastasis-associated protein 1 (MTA1) induced by pterostilbene (PTER) in hepatocellular carcinoma (HCC). The SMMC-7721 hepatoma cell line was treated with PTER. Following treatment, the mRNA transcript abundance of MTA1 was measured using quantitative polymerase chain reaction. Additionally, cell viability was determined using an MTT assay, and protein expression was measured through western blotting. Cell invasion, motility and apoptosis, as well as the cell cycle, were also investigated. Following PTER treatment, MTA1, histone deacetylase (HDAC) 1 and HDAC2 were downregulated, whereas the ratio of acetyl-p53 to total p53 was increased in HCC cells. Cell viability decreased as the PTER dose increased. MTA1 may be associated with proliferation, motility, invasion and metastasis in HCC cells. PTER appeared to repress cell proliferation, trigger apoptosis, induce cell cycle arrest, and inhibit motility and invasion via MTA1 in human liver cancer cells. The results of the present study demonstrated that PTER can downregulate the MTA1-nucleosome remodeling and deacetylase complex, and enhance p53 acetylation to inhibit the growth of tumor cells in HCC.
机译:本研究的目的是评估由蝶呤(PTER)诱导的转移相关蛋白1(MTA1)在肝细胞癌(HCC)中的杀肿瘤作用。用PTER处理SMMC-7721肝癌细胞系。处理后,使用定量聚合酶链反应测量MTA1的mRNA转录丰度。另外,使用MTT测定法测定细胞活力,并通过蛋白质印迹法测定蛋白质表达。还研究了细胞侵袭,运动性和凋亡以及细胞周期。 PTER处理后,MTA1,组蛋白脱乙酰基酶(HDAC)1和HDAC2被下调,而HCC细胞中乙酰基p53与总p53的比例增加。细胞活力随着PTER剂量的增加而降低。 MTA1可能与HCC细胞的增殖,运动,侵袭和转移有关。 PTER似乎可以抑制人肝癌细胞中的细胞增殖,触发细胞凋亡,诱导细胞周期停滞,并通过MTA1抑制运动性和侵袭。本研究的结果表明,PTER可以下调MTA1-核小体的重塑和脱乙酰基酶复合物,并增强p53乙酰化,从而抑制HCC中肿瘤细胞的生长。

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