Co-delivery of AKT3 siRNA and PTEN Plasmid by Antioxidant Nanoliposomes for Enhanced Antiproliferation of Prostate Cancer Cells,ACS Applied Bio Materials

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Co-delivery of AKT3 siRNA and PTEN Plasmid by Antioxidant Nanoliposomes for Enhanced Antiproliferation of Prostate Cancer Cells
ACS Applied Bio Materials ( IF 4.6 ) Pub Date : 2020-04-06 , DOI: 10.1021/acsabm.9b01016
Stuti Bhagat ₁ , Sanjay Singh ₁

Affiliation

Globally, prostate cancer is the fifth major cancer type and the second leading cause of cancer-related death in men. In 2018, about 1.3 million prostate cancer cases were reported worldwide. It is reported that loss of PTEN (tumor suppressor gene) expression leads to hyperactivation of the PI3K/AKT pathway and thus induces uncontrolled cell proliferation. Loss or mutation in regular PTEN expression is reported to occur in ∼30% of primary prostate cancer cases and ∼65% of metastatic cancer cases. Restoring the PTEN expression could inhibit the PI3K/AKT/mTOR signaling pathway, thus avoid the growth of prostate cancer cells. In this work, we have synthesized a multifunctional nanoliposomal formulation incorporating PTEN plasmid, AKT3 siRNA, and antioxidant cerium oxide nanoparticles (CeNPs). The nanoliposomes were able to successfully internalize in prostate cancer (PC-3) cells, restore the expression of PTEN protein, and knock down AKT3 mRNA. Further, the multifunctional nanoliposomes induce DNA damage and apoptosis in prostate cancer cells. The investigation of the PI3K/AKT/mTOR signaling pathway revealed that PTEN protein and apoptosis-specific proteins are overexpressed, leading to the inhibition of oncoproteins and, thus, prostate cancer.

中文翻译：

通过抗氧化纳米脂质体共同递送 AKT3 siRNA 和 PTEN 质粒以增强前列腺癌细胞的抗增殖作用

在全球范围内，前列腺癌是第五大癌症类型，也是男性癌症相关死亡的第二大原因。2018 年，全球报告了约 130 万例前列腺癌病例。据报道，PTEN（肿瘤抑制基因）表达的丧失导致 PI3K/AKT 通路的过度激活，从而诱导不受控制的细胞增殖。据报道，约 30% 的原发性前列腺癌病例和 65% 的转移性癌症病例中发生常规 PTEN 表达的缺失或突变。恢复PTEN表达可以抑制PI3K/AKT/mTOR信号通路，从而避免前列腺癌细胞的生长。在这项工作中，我们合成了一种包含 PTEN 质粒、AKT3 siRNA 和抗氧化铈氧化物纳米粒子 (CeNPs) 的多功能纳米脂质体制剂。纳米脂质体能够成功地在前列腺癌 (PC-3) 细胞中内化，恢复 PTEN 蛋白的表达，并敲低 AKT3 mRNA。此外，多功能纳米脂质体在前列腺癌细胞中诱导 DNA 损伤和凋亡。对 PI3K/AKT/mTOR 信号通路的研究表明，PTEN 蛋白和凋亡特异性蛋白过表达，导致癌蛋白抑制，从而抑制前列腺癌。

更新日期：2020-04-06

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