Department of Scienze della Vita e dell'Ambiente, Sezione di Scienze del Farmaco, University of Cagliari, Via Ospedale 72, 09124 Cagliari, Italy.
Department of Scienze, University of Basilicata, Viale dell'Ateneo Lucano 10, 85100 Potenza, Italy.
Int J Mol Sci. 2023 Feb 25;24(5):4552. doi: 10.3390/ijms24054552.
Liver cancer is one of the most common causes of cancer death worldwide. In recent years, substantial progress has been made in the development of systemic therapies, but there is still the need for new drugs and technologies that can increase the survival and quality of life of patients. The present investigation reports the development of a liposomal formulation of a carbamate molecule, reported as ANP0903, previously tested as an inhibitor of HIV-1 protease and now evaluated for its ability to induce cytotoxicity in hepatocellular carcinoma cell lines. PEGylated liposomes were prepared and characterized. Small, oligolamellar vesicles were produced, as demonstrated by light scattering results and TEM images. The physical stability of the vesicles in biological fluids was demonstrated in vitro, alongside the stability during storage. An enhanced cellular uptake was verified in HepG2 cells treated with liposomal ANP0903, resulting in a greater cytotoxicity. Several biological assays were performed to elucidate the molecular mechanisms explaining the proapoptotic effect of ANP0903. Our results allow us to hypothesize that the cytotoxic action in tumor cells is probably due to the inhibition of the proteasome, resulting in an increase in the amount of ubiquitinated proteins within the cells, which in turn triggers activation of autophagy and apoptosis processes, resulting in cell death. The proposed liposomal formulation represents a promising approach to deliver a novel antitumor agent to cancer cells and enhance its activity.
肝癌是全球癌症死亡的主要原因之一。近年来,在开发系统治疗方法方面取得了重大进展,但仍需要新的药物和技术来提高患者的生存率和生活质量。本研究报告了一种氨基甲酸酯类化合物的脂质体制剂的开发,该化合物先前被测试为 HIV-1 蛋白酶抑制剂,现在评估其在肝癌细胞系中诱导细胞毒性的能力。制备并表征了聚乙二醇化脂质体。如光散射结果和 TEM 图像所示,产生了小的、寡层状囊泡。体外证明了囊泡在生物流体中的物理稳定性,以及在储存过程中的稳定性。在用脂质体 ANP0903 处理的 HepG2 细胞中验证了增强的细胞摄取,导致更大的细胞毒性。进行了几项生物学测定,以阐明解释 ANP0903 促凋亡作用的分子机制。我们的结果使我们假设,肿瘤细胞中的细胞毒性作用可能是由于蛋白酶体的抑制,导致细胞内泛素化蛋白的量增加,进而触发自噬和细胞凋亡过程的激活,导致细胞死亡。所提出的脂质体制剂代表了向癌细胞递送新型抗肿瘤剂并增强其活性的有前途的方法。