Studies have shown that swertiamarin (STM) has multiple biological activities, but its anti-tumour effects and molecular mechanisms are still unclear. The present research aimed to validate the STM’s impacts on the proliferation, migration, and invasion of hepatocellular carcinoma (HCC) cells, and to study its potential mechanism. Two HCC cell lines were treated with STM. Tumour growth was observed by the mouse tumour xenografts model. HCC cell lines stably expressing T-cell lymphomas 1 (FRAT1) were generated by lentivirusmediated overexpression. Cell viability, proliferation, migration, and invasion were observed using Cell Counting Kit-8 (CCK8), the xCELLigence Real-Time Cell Analyzer system (RTCA), and transwell analysis, respectively. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting were used to observe the expression of FRAT1 and proteins related to the Wnt/β-catenin signalling pathway. Tumour growth was inhibited by STM in vivo. STM suppressed the proliferation, migration, and invasion of HCC cells. STM negatively regulated FRAT1 expression, whereas overexpressed FRAT1 blocked the anti-tumour function of STM. The results revealed that STM suppressed the FRAT1/Wnt/β-catenin signalling pathway. The findings of this study provide new insights into investigation of therapeutic strategies against HCC.

研究表明，swertiamarin（STM）具有多种生物学活性，但其抗肿瘤作用和分子机制仍不清楚。本研究旨在验证STM对肝细胞癌（HCC）细胞增殖，迁移和侵袭的影响，并研究其潜在机制。用STM处理两个HCC细胞系。通过小鼠肿瘤异种移植模型观察到肿瘤生长。慢病毒介导的过表达产生稳定表达T细胞淋巴瘤1（FRAT1）的HCC细胞系。分别使用Cell Counting Kit-8（CCK8），xCELLigence实时细胞分析仪系统（RTCA）和transwell分析观察了细胞活力，增殖，迁移和侵袭。定量实时聚合酶链反应（qRT-PCR）和蛋白质印迹用于观察FRAT1的表达和与Wnt /β-catenin信号通路相关的蛋白质。STM抑制肿瘤生长体内。STM抑制了HCC细胞的增殖，迁移和侵袭。STM负调节FRAT1的表达，而过表达的FRAT1阻止STM的抗肿瘤功能。结果表明，STM抑制FRAT1 / Wnt /β-catenin信号通路。这项研究的发现为抗HCC治疗策略的研究提供了新的见识。