Department of Respiratory Medicine, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing 210002, People's Republic of China.
Department of Respiratory Medicine, Jinling Hospital, Nanjing University of Chinese Medicine, Nanjing 210002, People's Republic of China.
ACS Appl Mater Interfaces. 2024 Oct 23;16(42):56910-56925. doi: 10.1021/acsami.4c15175. Epub 2024 Oct 14.
Cisplatin resistance significantly impacts the antitumor efficacy of cisplatin chemotherapy and contributes to poor prognosis, including metastasis. In this study, we present the utilization of metal-organic framework (MOF) nanoparticles as the therapeutic component and drug loading scaffold for implementing a ternary combination therapeutic strategy to combat cisplatin-resistant lung cancer and metastasis. Specifically, by engineering MOFs (Cis@MOF-siVEGF) through the self-assembly of THPP as photosensitizer for photodynamic therapy (PDT), along with the incorporation of cisplatin (DDP) and VEGF siRNA (siVEGF), we propose the leverage of photodynamic-induced oxidative damage and gene silencing of the angiogenic factor to reverse cisplatin resistance and sensitize therapeutic potency. Our findings demonstrated that the chemo/photodynamic/antiangiogenic triple combination therapy via Cis@MOF-siVEGF under irradiation effectively inhibits cisplatin-resistant tumor growth and induces abscopal effects. Importantly, molecular mechanistic exploration suggested that MUC4 exerted regulatory effects on governing cancer metastasis, thus representing a potential immunotherapeutic target for cancer intervention. Overall, our study creates a MOFs-based multicomponent delivery platform for complementary therapeutic modules with synergistically enhanced antitumor efficacy and sheds light on potential regulatory mechanisms on cisplatin-resistance cancers.
顺铂耐药显著影响顺铂化疗的抗肿瘤疗效,并导致预后不良,包括转移。在这项研究中,我们提出利用金属有机骨架(MOF)纳米粒子作为治疗成分和药物负载支架,实施三元组合治疗策略,以对抗顺铂耐药肺癌和转移。具体来说,通过 THPP 作为光敏剂用于光动力疗法(PDT)的自组装工程化 MOF(Cis@MOF-siVEGF),同时掺入顺铂(DDP)和 VEGF siRNA(siVEGF),我们提出利用光动力诱导的氧化损伤和血管生成因子的基因沉默来逆转顺铂耐药并增强治疗效力。我们的研究结果表明,通过 Cis@MOF-siVEGF 进行的化学/光动力/抗血管生成三联组合治疗在照射下可有效抑制顺铂耐药肿瘤的生长并诱导远隔效应。重要的是,分子机制探索表明 MUC4 对调控癌症转移具有调节作用,因此代表了癌症干预的潜在免疫治疗靶标。总的来说,我们的研究为互补治疗模块创建了基于 MOF 的多组分递送平台,具有协同增强的抗肿瘤疗效,并为顺铂耐药癌症的潜在调节机制提供了线索。