Department of General Surgery, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710004, P.R. China.
Oncol Rep. 2019 Jan;41(1):369-376. doi: 10.3892/or.2018.6786. Epub 2018 Oct 12.
Liver cancer is one of the most devastating types of cancer worldwide. Despite years of improvements in treatment, the prognosis of patients with this type of malignancy remains poor due to frequent recurrence and metastasis after surgical resection. Ginkgolic acid (GA) is a botanical drug extracted from the seed coat of Ginkgo biloba L. that possesses a wide range of bioactive properties. However, to the best of our knowledge, whether GA can inhibit the invasion of liver cancer cells and the underlying mechanisms remains unknown. The aim of the present study was to investigate the effects of GA on the migration and invasion abilities of liver cancer cells and the underlying molecular mechanism. The results revealed that GA suppressed the migration and invasion abilities of HepG2 cells. In addition, GA treatment inhibited the expression of invasion‑related molecules (MMP‑2 and MMP‑9) and prevented the epithelial‑mesenchymal transition (EMT) of HepG2 cells. Further experiments revealed that GA‑reduced hepatocyte growth factor (HGF) production and suppressed c‑Met phosphorylation may be the underlying mechanisms. Exogenous recombinant HGF supplementation improved the cell invasion ability impaired by GA. Moreover, the in vivo experiment revealed that GA inhibited the tumor growth of liver cancer and prevented EMT. Collectively, these data indicated that GA effectively suppressed the invasion and EMT of HepG2 cells via downregulation of HGF/c‑Met signaling, thus GA may serve as a novel chemotherapeutic agent for the treatment of HCC.
肝癌是全球最具破坏性的癌症之一。尽管在治疗方面取得了多年的进展,但由于手术后频繁复发和转移,此类恶性肿瘤患者的预后仍然不佳。银杏酸(GA)是从银杏种子的种皮中提取的植物药物,具有广泛的生物活性。然而,据我们所知,GA 是否能抑制肝癌细胞的侵袭以及潜在的机制尚不清楚。本研究旨在探讨 GA 对肝癌细胞迁移和侵袭能力的影响及其潜在的分子机制。结果表明,GA 抑制了 HepG2 细胞的迁移和侵袭能力。此外,GA 处理抑制了侵袭相关分子(MMP-2 和 MMP-9)的表达,并阻止了 HepG2 细胞的上皮-间充质转化(EMT)。进一步的实验表明,GA 减少了肝细胞生长因子(HGF)的产生并抑制了 c-Met 磷酸化可能是其潜在的机制。外源性重组 HGF 补充改善了 GA 引起的细胞侵袭能力受损。此外,体内实验表明,GA 抑制了肝癌的肿瘤生长并阻止了 EMT。综上所述,这些数据表明,GA 通过下调 HGF/c-Met 信号通路有效抑制了 HepG2 细胞的侵袭和 EMT,因此 GA 可能成为治疗 HCC 的新型化疗药物。