Evodiamine is an active alkaloid member found in Traditional Chinese Herb (TCH) Evodia rutaecarpa. It has been reported to exhibit remarkable biological and medicinal activities including anticancer and anti-inflammatory. This study was designed to investigate the anticancer effects of evodiamine against human liver cancer and evaluate its effects on cell migration, cell invasion, cellular apoptosis and PI3K/AKT pathway. The results showed that evodiamine exhibits potent antiproliferative effects against two human liver cancer cell lines (HepG2 and PLHC-1) with an IC50 of 20 µM. Nonetheless, the cytotoxic effects of evodiamine were comparatively low against the normal cells as evident from the IC50 of 100 μM. The growth inhibitory effects of evodiamine were found to be due to the induction of apoptosis as revealed by the DAPI, AO/EB and annexin V/PI staining assays. The induction of apoptosis was also associated with upregulation of Bax and downregulation of Bcl-2 expression in a concentration dependent manner. The wound healing and transwell assay revealed that evodiamine caused a significant decline in the migration and invasion of the HepG2 and PLHC-1 cells. Investigation of the effects of evodiamine on the PI3K/AKT signalling revealed that evodiamine inhibited the phosphorylation of PI3K and AKT proteins. Taken together, the results showed that evodiamine inhibits the growth of human liver cancer via induction of apoptosis and deactivation of PI3K/AKT pathway. The results point towards the therapeutic potential of evodiamine in the treatment of liver cancer.

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依维他命抑制人肝癌细胞生长涉及细胞凋亡和PI3K / AKT途径的失活

Evodiamine是在传统中草药Evodia rutaecarpa中发现的活性生物碱成员。据报道其具有显着的生物学和医学活性，包括抗癌和抗炎作用。这项研究旨在研究依维他命对人肝癌的抗癌作用，并评估其对细胞迁移，细胞侵袭，细胞凋亡和PI3K / AKT途径的影响。结果表明，依维他命对两种人类肝癌细胞系（HepG2和PLHC-1）具有有效的抗增殖作用，IC50为20 µM。但是，从100μM的IC50可以看出，依维多明对正常细胞的细胞毒性作用相对较低。如DAPI所揭示，发现依维他命的生长抑制作用是由于诱导细胞凋亡，AO / EB和膜联蛋白V / PI染色测定。凋亡的诱导还以浓度依赖性方式与Bax的上调和Bcl-2表达的下调相关。伤口愈合和transwell分析表明，依维他命引起HepG2和PLHC-1细胞迁移和侵袭的显着下降。依夫二胺对PI3K / AKT信号传导的影响研究表明，依夫二胺抑制PI3K和AKT蛋白的磷酸化。两者合计，结果表明，依维他命通过诱导细胞凋亡和PI3K / AKT通路的失活抑制人肝癌的生长。研究结果表明依维他命具有治疗肝癌的潜力。凋亡的诱导还以浓度依赖性方式与Bax的上调和Bcl-2表达的下调相关。伤口愈合和transwell分析表明，依维他命引起HepG2和PLHC-1细胞迁移和侵袭的显着下降。依夫二胺对PI3K / AKT信号传导的影响研究表明，依夫二胺抑制PI3K和AKT蛋白的磷酸化。两者合计，结果表明，依维他命通过诱导细胞凋亡和PI3K / AKT通路的失活抑制人肝癌的生长。研究结果表明依维他命具有治疗肝癌的潜力。凋亡的诱导还以浓度依赖性方式与Bax的上调和Bcl-2表达的下调相关。伤口愈合和transwell分析表明，依维他命引起HepG2和PLHC-1细胞迁移和侵袭的显着下降。依夫二胺对PI3K / AKT信号传导的影响研究表明，依夫二胺抑制PI3K和AKT蛋白的磷酸化。两者合计，结果表明，依维他命通过诱导细胞凋亡和PI3K / AKT通路的失活抑制人肝癌的生长。研究结果表明依维他命具有治疗肝癌的潜力。伤口愈合和transwell分析表明，依维他命引起HepG2和PLHC-1细胞迁移和侵袭的显着下降。依夫二胺对PI3K / AKT信号传导的影响研究表明，依夫二胺抑制PI3K和AKT蛋白的磷酸化。两者合计，结果表明，依维他命通过诱导细胞凋亡和PI3K / AKT通路的失活抑制人肝癌的生长。研究结果表明依维他命具有治疗肝癌的潜力。伤口愈合和transwell分析表明，依维他命引起HepG2和PLHC-1细胞迁移和侵袭的显着下降。依夫二胺对PI3K / AKT信号传导的影响研究表明，依夫二胺抑制PI3K和AKT蛋白的磷酸化。两者合计，结果表明，依维他命通过诱导细胞凋亡和PI3K / AKT通路的失活抑制人肝癌的生长。研究结果表明依维他命具有治疗肝癌的潜力。结果表明，依地洛明通过诱导细胞凋亡和PI3K / AKT通路失活来抑制人肝癌的生长。研究结果表明依维他命具有治疗肝癌的潜力。结果表明，依地洛明通过诱导细胞凋亡和PI3K / AKT通路失活来抑制人肝癌的生长。研究结果表明依维他命具有治疗肝癌的潜力。