Liver cancer had become the sixth most common cancer. Nitidine chloride (NC) has demonstrated promising anti-HCC properties; however, further elucidation of its mechanism of action is necessary. The anti-HCC targets of NC were identified through the utilization of multiple databases and ChIPs data analysis. The GO and KEGG analyses to determine the specific pathway affected by NC. The Huh 7 and Hep G2 cells were subjected to a 24-h treatment with NC, followed by evaluating the impact of NC on cell proliferation and cell cycle. The involvement of the p53/14-3-3 Sigma/CDK1 axis in HCC cells was confirmed by qPCR and WB analysis of the corresponding genes and proteins. The GO and KEGG analysis showed the targets were related to cell cycle and p53 signaling pathways. In vitro experiments showed that NC significantly inhibited the proliferation of HCC cells and induced G2/M phase arrest. In addition, qPCR and WB experiments showed that the expression of p53 in HCC cells increased after NC intervention, while the expression of 14-3-3 Sigma and CDK1 decreased. NC can inhibit the proliferation of HCC cells and induce G2/M cell cycle arrest, potentially by regulating the p53/14-3-3 Sigma/CDK1 axis

中文翻译：

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氯化两面针碱通过调节 p53/14-3-3 Sigma/CDK1 轴抑制 G2/M 期用于肝细胞癌治疗


肝癌已成为第六大常见癌症。氯化两面针碱 (NC) 已被证明具有良好的抗 HCC 特性；然而，有必要进一步阐明其作用机制。通过利用多个数据库和 ChIP 数据分析来确定 NC 的抗 HCC 靶点。 GO 和 KEGG 分析以确定受 NC 影响的具体途径。 Huh 7和Hep G2细胞用NC处理24小时，然后评估NC对细胞增殖和细胞周期的影响。通过 qPCR 和相应基因和蛋白质的 WB 分析证实了 p53/14-3-3 Sigma/CDK1 轴在 HCC 细胞中的参与。 GO和KEGG分析显示靶点与细胞周期和p53信号通路相关。体外实验表明NC显着抑制HCC细胞增殖并诱导G2/M期阻滞。此外，qPCR和WB实验表明，NC干预后HCC细胞中p53的表达增加，而14-3-3 Sigma和CDK1的表达减少。 NC 可能通过调节 p53/14-3-3 Sigma/CDK1 轴抑制 HCC 细胞增殖并诱导 G2/M 细胞周期停滞