肝细胞癌（HCC）由于早期复发和其转移特征而与高死亡率相关。到目前为止，对转移性HCC的有效治疗选项仍是患者治疗的一个主要挑战。黄连素B（FKB）是一种天然存在的香豆素分子，能够为这种威胁生命的疾病提供有效的治疗。本研究调查了FKB对转移性HCC生长和发展的抗转移效果。本研究使用了HepG2细胞，并进行了中性红染色法来确定FKB的IC50值。细胞划痕和排斥区实验被用来评估细胞迁移和侵袭的速率。使用RT-qPCR测定了UCK2、STAT3、VEGF和HIF-1α基因的相对mRNA水平。FKB在72小时孵育后以28µM的IC50值抑制了HepG2细胞的增殖。其细胞毒性效应通过相差相衬显微镜证实能够通过凋亡诱导。相比未处理的细胞，FKB在7、14和28µM浓度下显著抑制了细胞迁移和侵袭。细胞迁移的抑制随着生物活性化合物浓度的增加而显著增加。经过72小时FKB处理后，UCK2基因及其下游基因STAT3、VEGF和HIF-1α的相对表达水平显著下调。我们的数据表明，FKB通过调节STAT3/Hif-1α/VEGF信号通路，抑制了HepG2的增殖并进一步抑制了其转移。FKB可能是一种潜在的替代和可行的抗HCC策略。版权所有© Bentham Science Publishers；如有任何问题，请发送电子邮件至epub@benthamscience.net。

Hepatocellular carcinoma (HCC) is associated with a high mortality rate due to early recurrence and its metastasis features. To this day, effective treatment options for metastatic HCC remain a major challenge to patient treatment. Flavokawain B (FKB) is a naturally occurring chalcone molecule capable of providing effective therapy against this life-threatening disease.This study investigated the anti-metastatic effects of FKB on the growth and development of metastatic HCC.HepG2 cells were used in this study and a neutral red assay was performed to determine the IC50 value of FKB. Cell scratch and exclusion zone assays were performed to assess the rate of cell migration and invasion. Relative mRNA levels of UCK2, STAT3, VEGF and HIF-1α genes were quantified using RT-qPCR.FKB inhibited the proliferation of HepG2 cells at an IC50 value of 28 µM after 72 h of incubation. Its cytotoxic effect was confirmed to induce apoptosis through the phase-contrast inverted microscope. Cell migration and invasion were significantly inhibited at 7, 14, and 28 µM of FKB as compared to untreated cells. The inhibition in the cell migration significantly increased with the increasing concentrations of the bioactive compound. The relative expression levels of the UCK2 gene and its downstream genes, STAT3, VEGF and HIF-1α, were significantly downregulated after 72 h exposure to FKB treatment.Our data suggest that FKB inhibited HepG2 proliferation and further suppressed its metastasis partly by regulating the STAT3/Hif-1α/VEGF signalling pathway. FKB could be a potential alternative and viable strategy against HCC.Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.