In view of the tumor-inhibiting effect of α-santalol in various cancers and the role of E2F transcription factor 1 (E2F1) as an important target for anticancer research, this study investigates the relation between α-santalol and E2F1, as well as the effect of α-santalol on liver cancer progression and the corresponding mechanism. Concretely, liver cancer cells were treated with different concentrations of α-santalol. The IC₅₀ value of α-santalol was determined using Probit regression analysis. Then, transcription factors that are targeted by α-santalol and differentially expressed in liver cancer were screened out. The clinicopathological impact of E2F1 and its targets were evaluated and predicted. The expressions of E2F1 and high-mobility group box 2 (HMGB2) and their correlation in the liver cancer tissues were analyzed by bioinformatics. The effects of E2F1 and HMGB2 on the biological characteristics of liver cancer cells were examined through loss/gain-of-function and molecular assays. With the extension of treatment time, the inhibitory effects of 10 μmol/L and 20 μmol/L α-santalol on cancer cell survival rate were enhanced (P<0.001). E2F1 and HMGB2 were highly expressed and positively correlated in liver cancer tissues (P<0.05). High E2F1 expression was correlated with large tumors and high TNM stages (P<0.05). E2F1 knockdown promoted the effects of α-santalol on dose-dependently inhibiting viability, colony formation, invasion and migration (P<0.05). Moreover, E2F1 knockdown reduced the IC₅₀ value and HMGB2 level, while HMGB2 overexpression produced opposite effects. HMGB2 overexpression and E2F1 knockdown mutually counteracted their effects on the IC₅₀ value and on the viability and apoptosis of α-santalol-treated liver cancer cells (P<0.01). Collectively, blocking the E2F1/HMGB2 pathway enhances the intervention effects of α-santalol on the proliferation, migration and invasion of liver cancer cells.

鉴于α-檀香醇在多种癌症中的抑瘤作用以及E2F转录因子1（E2F1）作为抗癌研究重要靶点的作用，本研究探讨了α-檀香醇与E2F1之间的关系，以及E2F1与E2F1的关系。 α-檀香醇对肝癌进展的影响及其机制。具体来说，用不同浓度的α-檀香醇处理肝癌细胞。使用Probit回归分析确定α-檀香醇的IC _50值。然后，筛选出α-檀香醇靶向的、在肝癌中差异表达的转录因子。评估和预测了E2F1及其靶点的临床病理影响。采用生物信息学方法分析肝癌组织中E2F1和高迁移率族蛋白2( HMGB2 )的表达情况及其相关性。通过功能丧失/获得和分子测定来检查E2F1和HMGB2对肝癌细胞生物学特性的影响。随着治疗时间的延长，10 μmol/L和20 μmol/L α-檀香醇对癌细胞存活率的抑制作用增强（P <0.001）。E2F1、HMGB2在肝癌组织中高表达且呈正相关（P <0.05）。E2F1高表达与肿瘤大和 TNM 分期高相关（P <0.05）。E2F1敲除促进 α-檀香醇剂量依赖性抑制活力、集落形成、侵袭和迁移的作用（P <0.05）。此外，E2F1敲低降低了IC ₅₀值和HMGB2水平，而HMGB2过表达产生相反的效果。HMGB2过表达和E2F1敲低相互抵消了它们对α-檀香醇处理的肝癌细胞的IC _{50值以及活力和凋亡的影响（} P <0.01）。总的来说，阻断E2F1 / HMGB2通路增强了α-檀香醇对肝癌细胞增殖、迁移和侵袭的干预作用。