Department of Pharmaceutics and Biopharmaceutics, University of Marburg, Marburg, Germany.
Department of Chemistry, Angström Laboratory, Uppsala University, Uppsala, Sweden.
Drug Deliv. 2022 Dec;29(1):2072-2085. doi: 10.1080/10717544.2022.2092234.
Hypoxia, an oxygen-deprived condition of the tumor, is one of the major reasons for resistance to chemotherapy. Carbonic anhydrases are generally involved in pH homeostasis in normal conditions, but in solid tumors having a strong relation with hypoxia, the carbonic anhydrase IX (CA-IX) enzyme is overexpressed and results in an extracellular acidic environment. For most weakly basic anticancer drugs, including doxorubicin (Dox), the ionization in an acidic environment limits their cellular uptake, and consequently, the tumor exposure to the drug at sub-therapeutic concentration comes out as chemoresistance. Herein, a combined drug delivery system of liposomes and mesoporous silica nanoparticles (MSNPs) was developed for the co-delivery of the CA-IX enzyme inhibitor and Dox in hypoxic condition. The unique structure of MSNPs with higher surface area was utilized for higher drug loading and sustained release of Dox. Additionally, the biocompatible nature of liposomal coating as a second loading site for the CA-IX enzyme inhibitor has provided gatekeeping effects at pore opening to avoid premature drug release. Lipid coated MSNPs as a co-delivery system for Dox and the CA-IX inhibitor have synergistic cytotoxic effects against MDA-MB 231 breast cancer cells in hypoxic conditions. These findings assure the potential of this drug delivery system to overcome hypoxia-related chemoresistance.
缺氧是肿瘤化疗耐药的主要原因之一,它是肿瘤缺氧的一种情况。碳酸酐酶通常参与正常条件下的 pH 平衡,但在与缺氧密切相关的实体瘤中,碳酸酐酶 IX(CA-IX)酶过表达,导致细胞外环境呈酸性。对于大多数弱碱性抗癌药物,包括阿霉素(Dox),在酸性环境下的离子化会限制其细胞摄取,因此,药物在低于治疗浓度的情况下进入肿瘤,导致化疗耐药。在此,开发了一种脂质体和介孔硅纳米粒子(MSNPs)的联合药物传递系统,用于在缺氧条件下共递送 CA-IX 酶抑制剂和 Dox。MSNPs 具有更高的表面积,利用其独特的结构可以实现更高的药物载药量和 Dox 的持续释放。此外,脂质体涂层作为 CA-IX 酶抑制剂的第二个载药部位,具有生物相容性,可以在孔打开时提供门控效应,以避免药物过早释放。脂质体包裹的 MSNPs 作为 Dox 和 CA-IX 抑制剂的共递药系统,对 MDA-MB 231 乳腺癌细胞在缺氧条件下具有协同细胞毒性作用。这些发现证实了这种药物传递系统克服与缺氧相关的化疗耐药的潜力。