Faculty of Medicine, The University of Queensland, Brisbane, QLD 4120, Australia.
Gallipoli Medical Research Institute, Greenslopes Private Hospital, Brisbane, QLD 4120, Australia.
Curr Oncol. 2021 Jun 11;28(3):2150-2172. doi: 10.3390/curroncol28030200.
Sorafenib, an oral multi-tyrosine kinase inhibitor, has been the first-line therapy for the treatment of patients with advanced HCC, providing a survival benefit of only three months in approximately 30% of patients. Cancer stem cells (CSCs) are a rare tumour subpopulation with self-renewal and differentiation capabilities, and have been implicated in tumour growth, recurrence and drug resistance. The process of epithelial-to-mesenchymal transition (EMT) contributes to the generation and maintenance of the CSC population, resulting in immune evasion and therapy resistance in several cancers, including HCC. The aim of this study is to target the chemoresistant CSC population in HCC by assessing the effectiveness of a combination treatment approach with Sorafenib, an EMT inhibitor and an immune checkpoint inhibitor (ICI). A stem-cell-conditioned serum-free medium was utilised to enrich the CSC population from the human HCC cell lines Hep3B, PLC/PRF/5 and HepG2. The anchorage independent spheres were characterised for CSC features. The human HCC-derived spheres were assessed for EMT status and expression of immune checkpoint molecules. The effect of combination treatment with SB431542, an EMT inhibitor, and siRNA-mediated knockdown of programmed cell death protein ligand-1 (PD-L1) or CD73 along with Sorafenib on human HCC-derived CSCs was examined with cell viability and apoptosis assays. The three-dimensional spheres enriched from human HCC cell lines demonstrated CSC-like features. The human HCC-derived CSCs also exhibited the EMT phenotype along with the upregulation of immune checkpoint molecules. The combined treatment with SB431542 and siRNA-mediated PD-L1 or CD73 knockdown effectively enhanced the cytotoxicity of Sorafenib against the CSC population compared to Sorafenib alone, as evidenced by the reduced size and proliferation of spheres. Furthermore, the combination treatment of Sorafenib with SB431542 and PD-L1 or CD73 siRNA resulted in an increased proportion of an apoptotic population, as evidenced by flow cytometry analysis. In conclusion, the combined targeting of EMT and immune checkpoint molecules with Sorafenib can effectively target the CSC tumour subpopulation.
索拉非尼是一种口服多酪氨酸激酶抑制剂,已成为治疗晚期 HCC 患者的一线治疗药物,约 30%的患者的生存获益仅为 3 个月。癌症干细胞(CSC)是一种具有自我更新和分化能力的罕见肿瘤亚群,已被牵涉到肿瘤的生长、复发和耐药性中。上皮间质转化(EMT)过程有助于 CSC 群体的产生和维持,导致包括 HCC 在内的几种癌症的免疫逃避和治疗耐药。本研究的目的是通过评估索拉非尼、EMT 抑制剂和免疫检查点抑制剂(ICI)联合治疗方案对 HCC 耐药 CSC 群体的有效性,来靶向治疗 HCC 耐药 CSC 群体。利用无血清条件培养基从人 HCC 细胞系 Hep3B、PLC/PRF/5 和 HepG2 中富集 CSC 群体。对无附着球体进行 CSC 特征分析。评估人 HCC 衍生球体的 EMT 状态和免疫检查点分子的表达。通过细胞活力和凋亡测定法,研究了 SB431542(EMT 抑制剂)与 siRNA 介导的程序性死亡配体 1(PD-L1)或 CD73 敲低联合索拉非尼对人 HCC 衍生 CSC 的联合治疗效果。从人 HCC 细胞系富集的三维球体显示出 CSC 样特征。人 HCC 衍生的 CSCs 也表现出 EMT 表型,并上调免疫检查点分子。与单独使用索拉非尼相比,SB431542 和 siRNA 介导的 PD-L1 或 CD73 敲低联合治疗可有效增强索拉非尼对 CSC 群体的细胞毒性,这体现在球体的大小和增殖减少上。此外,索拉非尼与 SB431542 和 PD-L1 或 CD73 siRNA 的联合治疗导致凋亡群体的比例增加,这通过流式细胞术分析得到证实。总之,索拉非尼联合 EMT 和免疫检查点分子的联合靶向治疗可有效靶向 CSC 肿瘤亚群。