Lupin Ltd, 46/47, A, Village Nande, Taluka Mulshi Dist, Pune 412 115, India(1).
INSYS Therapeutics, 444 S Ellis St and 410 S Benson Ln, Chandler, AZ 85224, USA(1).
Int J Pharm. 2018 May 30;543(1-2):130-138. doi: 10.1016/j.ijpharm.2018.03.045. Epub 2018 Mar 27.
RNA interference has tremendous potential for cancer therapy but is limited by the insufficient potency of RNAi molecules after i.v. administration. We previously found that complexation with PLL(30)-PEG(5K) greatly increases the potency of 3'-cholesterol-modified siRNA [Chol-siRNA] in primary murine syngeneic 4T1 breast tumors after i.v. administration but mRNA suppression decreases 24 h after the final dose. We hypothesized that complexation of cholesterol-modified Dicer-substrate siRNA (Chol-DsiRNA) in place of Chol-siRNA can increase the potency and duration of suppression by polyplexes of PLL(30)-PEG(5K) in solid tumors. We found that replacing Chol-siRNA with Chol-DsiRNA increased polyplex loading and nuclease protection, suppressed stably expressed luciferase to the same extent in primary murine 4T1-Luc breast tumors under the current dosage regimen, but maintained suppression ~72 h after the final dose. The kinetics of suppression in 4T1-Luc over 72 h, however, were similar between DsiLuc and siLuc after electroporation and between polyplexes of Chol-DsiLuc and Chol-siLuc after transfection, suggesting that Chol-DsiRNA polyplexes increase the duration of mRNA suppression through differences in polyplex activities in vivo. Thus, replacing Chol-siRNA with Chol-DsiRNA may significantly increase the duration of mRNA suppression by polyplexes of PLL(30)-PEG(5K) and possibly other PEGylated polycationic polymers in primary tumors and metastases after i.v. administration.
RNA 干扰在癌症治疗方面具有巨大的潜力,但由于静脉注射后 RNAi 分子的效力不足而受到限制。我们之前发现,用 PLL(30)-PEG(5K) 进行复合可大大提高静脉注射后 3'-胆固醇修饰的 siRNA [Chol-siRNA] 在原发性小鼠同基因 4T1 乳腺肿瘤中的效力,但 mRNA 抑制在最后一次给药后 24 小时下降。我们假设用胆固醇修饰的 Dicer 底物 siRNA (Chol-DsiRNA) 代替 Chol-siRNA 进行复合,可以通过 PLL(30)-PEG(5K) 的多聚物增加实体瘤中抑制的效力和持续时间。我们发现,用 Chol-DsiRNA 代替 Chol-siRNA 可以增加多聚物的负载和核酸酶保护,在当前剂量方案下,在原发性小鼠 4T1-Luc 乳腺肿瘤中稳定表达的荧光素酶抑制到相同程度,但在最后一次给药后仍能维持抑制作用~72 小时。然而,在电穿孔后,DsiLuc 和 siLuc 之间以及 Chol-DsiLuc 和 Chol-siLuc 多聚物之间,4T1-Luc 超过 72 小时的抑制动力学相似,这表明 Chol-DsiRNA 多聚物通过体内多聚物活性的差异增加了 mRNA 抑制的持续时间。因此,用 Chol-DsiRNA 代替 Chol-siRNA 可能会显著增加 PLL(30)-PEG(5K) 多聚物和可能其他经 PEG 化的聚阳离子聚合物在原发性肿瘤和转移瘤中的 mRNA 抑制持续时间。