Department of Pharmaceutical Sciences, University of Nebraska Medical Center, Omaha, Nebraska 68198, United States.
ACS Appl Mater Interfaces. 2024 Jun 12;16(23):29686-29698. doi: 10.1021/acsami.4c02626. Epub 2024 May 30.
Gemcitabine (GEM) is a nucleoside analogue approved as a first line of therapy for pancreatic ductal adenocarcinoma (PDAC). However, rapid metabolism by plasma cytidine deaminase leading to the short half-life, intricate intracellular metabolism, ineffective cell uptake, and swift development of chemoresistance downgrades the clinical efficacy of GEM. ONC201 is a small molecule that inhibits the Akt and ERK pathways and upregulates the TNF-related apoptosis-inducing ligand (TRAIL), which leads to the reversal of both intrinsic and acquired GEM resistance in PDAC treatment. Moreover, the pancreatic cancer cells that were able to bypass apoptosis after treatment of ONC201 get arrested in the G1-phase, which makes them highly sensitive to GEM. To enhance the in vivo stability of GEM, we first synthesized a disulfide bond containing stearate conjugated GEM (lipid-GEM), which makes it sensitive to the redox tumor microenvironment (TME) comprising high glutathione levels. In addition, with the help of colipids 1,2-dioleoyl-glycero-3-phosphocholine (DOPC), cholesterol, and 1,2-distearoyl-glycero-3-phosphoethanolamine-poly(ethylene glycol)-2000 (DSPE-PEG 2000), we were able to synthesize the lipid-GEM conjugate and ONC201 releasing liposomes. A cumulative drug release study confirmed that both ONC201 and GEM showed sustained release from the formulation. Since MUC1 is highly expressed in 70-90% PDAC, we conjugated a MUC1 binding peptide in the liposomes which showed higher cytotoxicity, apoptosis, and cellular internalization by MIA PaCa-2 cells. A biodistribution study further confirmed that the systemic delivery of the liposomes through the tail vein resulted in a higher accumulation of drugs in orthotopic PDAC tumors in NSG mice. The IHC of the excised tumor grafts further confirmed the higher apoptosis and lower metastasis and cell proliferation. Thus, our MUC1 targeting binary drug-releasing liposomal formulation showed higher drug payload, enhanced plasma stability, and accumulation of drugs in the pancreatic orthotopic tumor and thus is a promising therapeutic alternative for the treatment of PDAC.
吉西他滨(GEM)是一种核苷类似物,被批准作为胰腺导管腺癌(PDAC)的一线治疗药物。然而,由于血浆胞苷脱氨酶的快速代谢导致半衰期短、复杂的细胞内代谢、细胞摄取效率低以及快速产生化疗耐药性,降低了 GEM 的临床疗效。ONC201 是一种小分子,可抑制 Akt 和 ERK 通路,并上调 TNF 相关凋亡诱导配体(TRAIL),从而逆转 PDAC 治疗中内在和获得性的 GEM 耐药性。此外,在 ONC201 治疗后能够绕过细胞凋亡的胰腺癌细胞在 G1 期被阻滞,这使它们对 GEM 高度敏感。为了提高 GEM 的体内稳定性,我们首先合成了含有二硫键的硬脂酸共轭 GEM(脂质-GEM),使其对包含高谷胱甘肽水平的氧化还原肿瘤微环境(TME)敏感。此外,在 1,2-二油酰基-sn-甘油-3-磷酸胆碱(DOPC)、胆固醇和 1,2-二硬脂酰基-sn-甘油-3-磷酸乙醇胺聚乙二醇 2000(DSPE-PEG 2000)的帮助下,我们能够合成脂质-GEM 缀合物和释放 ONC201 的脂质体。累积药物释放研究证实,ONC201 和 GEM 均从制剂中持续释放。由于 MUC1 在 70-90%的 PDAC 中高度表达,我们在脂质体中缀合了一种 MUC1 结合肽,该肽在 MIA PaCa-2 细胞中显示出更高的细胞毒性、细胞凋亡和细胞内化。分布研究进一步证实,通过尾静脉系统递送脂质体导致在 NSG 小鼠的原位 PDAC 肿瘤中药物更高的积累。切除的肿瘤移植物的 IHC 进一步证实了更高的细胞凋亡、更低的转移和细胞增殖。因此,我们的 MUC1 靶向二元药物释放脂质体制剂显示出更高的药物载量、增强的血浆稳定性以及在胰腺原位肿瘤中的药物积累,因此是治疗 PDAC 的一种有前途的治疗选择。