Yamaji Megumi, Nakahara Tomomi, Nakanishi Tomoko, Aoyama-Kikawa Satomi, Yamaguchi Kiyoshi, Furukawa Yoichi, Nakamura Mariko, Okada Tadashi, Tabata Hirotaka, Fuse Ryoko, Shimizu Eigo, Kasajima Rika, Imoto Seiya, Kukimoto Iwao, Saito Izumu, Kiyono Tohru
Center of Biomedical Research Resources, Juntendo University School of Medicine, Tokyo 113-8421, Japan.
National Cancer Center Research Institute, Tokyo 466-0045, Japan.
Int J Mol Sci. 2025 Sep 5;26(17):8685. doi: 10.3390/ijms26178685.
Human papillomavirus (HPV) is a prime target for genome-editing therapy as its E6 and E7 oncogenes are crucial for cancer development and maintenance. A key challenge in CRISPR/Cas9 therapy is the off-target effects. This study utilized a double-nicking technique to introduce DNA breaks in the E6 and E7 regions of HPV16. From 146 gRNA candidates, 16 double-nicking pairs were selected. Multiple combinations of double-nicking (DN)-gRNA pairs were delivered to HPV16-positive cells via lentiviruses, followed by Cas9 nickase (Cas9n) expression. Combinations of 3-4 DN-gRNA pairs effectively killed HPV16-positive cells while sparing HPV-negative cells. Off-target effects were reduced by nearly three orders of magnitude. An "all-in-one" adenovirus (AdV) system expressing four gRNA pairs and Cas9n showed promise in inhibiting tumor growth in HPV16-positive cancer models, demonstrating its potential as a safe and effective treatment for HPV-induced tumors.
人乳头瘤病毒(HPV)是基因编辑治疗的主要靶点,因为其E6和E7癌基因对癌症的发生和维持至关重要。CRISPR/Cas9治疗中的一个关键挑战是脱靶效应。本研究利用双切口技术在HPV16的E6和E7区域引入DNA断裂。从146个gRNA候选序列中,选择了16对双切口序列。通过慢病毒将多组双切口(DN)-gRNA对递送至HPV16阳性细胞,随后表达Cas9切口酶(Cas9n)。3-4对DN-gRNA对的组合可有效杀死HPV16阳性细胞,同时不影响HPV阴性细胞。脱靶效应降低了近三个数量级。一种表达四对gRNA和Cas9n的“一体化”腺病毒(AdV)系统在抑制HPV16阳性癌症模型中的肿瘤生长方面显示出前景,证明了其作为HPV诱导肿瘤的安全有效治疗方法的潜力。