Kwak Minseo, Hua Truong Chinh, Jin Hyesoo, Lee Jongsam, Kim Dong-Eun
Department of Bioscience and Biotechnology, Konkuk University, Seoul 05029, Republic of Korea.
Int J Mol Sci. 2025 Aug 30;26(17):8467. doi: 10.3390/ijms26178467.
Pancreatic ductal adenocarcinoma (PDAC) is among the most lethal malignancies due to late diagnosis, poor drug penetration, and intrinsic chemoresistance. Targeted delivery strategies are urgently needed to enhance therapeutic precision while minimizing systemic toxicity. Here, we developed an AS1411 aptamer-functionalized liposomal platform encapsulating siRNA against metastasis-associated protein 2 (MTA2), a chromatin remodeling factor that suppresses the tumor suppressor PTEN and activates PI3K/AKT signaling. The AS1411 aptamer, which binds nucleolin overexpressed on PDAC cells, was conjugated to cationic liposomes via copper-free click chemistry. The resulting AS1411-Lipm[siRNA] exhibited high siRNA encapsulation efficiency, selective uptake by nucleolin-positive PDAC cells, and enhanced endosomal escape. Treatment of MIA PaCa-2 cells with AS1411-Lipm[siRNA] significantly reduced MTA2 expression by ~60%, substantially restored PTEN, and inhibited AKT phosphorylation by ~50%, leading to decreased cell viability, impaired migration by ~75%, and increased apoptosis by ~35%, while sparing nucleolin-negative cells. These findings highlight AS1411-Lipm[siRNA] as a promising platform for selective siRNA delivery and potent molecular inhibition in PDAC therapy.
胰腺导管腺癌(PDAC)是最致命的恶性肿瘤之一,原因在于诊断延迟、药物渗透性差以及内在的化疗耐药性。迫切需要靶向递送策略来提高治疗精准度,同时将全身毒性降至最低。在此,我们开发了一种AS1411适配体功能化的脂质体平台,该平台包裹着针对转移相关蛋白2(MTA2)的小干扰RNA(siRNA),MTA2是一种染色质重塑因子,可抑制肿瘤抑制因子PTEN并激活PI3K/AKT信号通路。与在PDAC细胞上过度表达的核仁素结合的AS1411适配体,通过无铜点击化学法与阳离子脂质体偶联。所得的AS1411-Lipm[siRNA]表现出高siRNA包封效率、被核仁素阳性的PDAC细胞选择性摄取以及增强的内体逃逸能力。用AS1411-Lipm[siRNA]处理MIA PaCa-2细胞可使MTA2表达显著降低约60%,使PTEN基本恢复,并使AKT磷酸化抑制约50%,导致细胞活力下降、迁移能力受损约75%以及凋亡增加约35%,同时对核仁素阴性细胞无影响。这些发现突出了AS1411-Lipm[siRNA]作为一种在PDAC治疗中用于选择性siRNA递送和有效分子抑制的有前景的平台。