Related experimental raw data of SMMC-7721.

ObjectiveThis study aimed to elucidate the effects of Hederagenin (HG) on hepatocellular carcinoma (HCC) and explore its potential molecular mechanisms.Materials and methodsVirtual screening was employed to identify potential targets within core pathways of liver cancer and to analyze the possible mechanisms of HG. CCK-8 assays were used to assess the viability of HCC cells, while Hoechst 33342/PI staining was utilized to evaluate apoptosis. The migration and invasion abilities of HCC cells were examined using Transwell and scratch assays, and single-cell cloning ability was assessed via colony formation assays. Subsequent qRT-PCR was conducted to determine the mRNA expression levels of FOXO1 and FOXO6 following HG treatment. Western blot (WB) analysis was employed to measure the protein expression levels of IGF1R, FOXO1, FOXO6, MMP2, MMP9, and VEGFA, as well as the phosphorylation status of FOXO1 Ser249.ResultsVirtual screening indicated that HG might exert antitumor effects through the FOXO signaling pathway. Experimental results demonstrated that HG induces apoptosis in a dose-dependent manner and inhibits the proliferation, migration, invasion, and single-cell cloning ability of HCC cells. After HG treatment, FOXO1 expression was upregulated, while the expression levels of IGF1R, phosphorylated FOXO1 Ser249, MMP2, MMP9, and VEGFA were downregulated.ConclusionIn summary, our study is the first to demonstrate that HG regulates the phosphorylation of FOXO1, affecting the proliferation, migration, and invasion of HCC cells. The findings suggest that HG can inhibit the migration of HCC cells in vitro. The data indicate that HG-mediated targeting of the FOXO1/FOXO6 pathway holds promise as a novel therapeutic approach.研究目的 本研究旨在阐明常春藤皂苷元（Hederagenin，HG）对肝细胞癌（hepatocellular carcinoma，HCC）的作用，并探索其潜在分子机制。 材料与方法 本研究通过虚拟筛选技术识别肝癌核心通路中的潜在靶点，分析HG的潜在作用机制。采用CCK-8实验检测肝细胞癌细胞的增殖活力；通过Hoechst 33342/PI染色法评估细胞凋亡情况；利用Transwell实验与划痕实验检测肝细胞癌细胞的迁移与侵袭能力；采用集落形成实验检测单细胞克隆能力。后续采用实时荧光定量PCR（qRT-PCR）检测HG处理后FOXO1与FOXO6的mRNA表达水平；采用蛋白质印迹（Western blot，WB）分析IGF1R、FOXO1、FOXO6、MMP2、MMP9及VEGFA的蛋白表达水平，以及FOXO1 Ser249的磷酸化状态。 结果 虚拟筛选结果显示，HG可能通过FOXO信号通路发挥抗肿瘤活性。实验结果表明，HG可诱导肝细胞癌细胞凋亡且呈剂量依赖性，同时可抑制癌细胞的增殖、迁移、侵袭及单细胞克隆能力。经HG处理后，FOXO1的表达水平显著上调，而IGF1R、磷酸化FOXO1 Ser249、MMP2、MMP9及VEGFA的表达水平均显著下调。 结论 综上，本研究首次证实HG可通过调控FOXO1的磷酸化水平，影响肝细胞癌细胞的增殖、迁移与侵袭能力。研究结果提示HG可在体外抑制肝细胞癌细胞的迁移。数据表明，HG靶向调控FOXO1/FOXO6通路有望成为肝细胞癌治疗的全新策略。