HPV-driven cancers: a looming threat and the potential of CRISPR/Cas9 for targeted therapy.

IF 4 3区 医学 Q2 VIROLOGY
Atefeh Zamani Kermanshahi, Fatemeh Ebrahimi, Ahmad Taherpoor, Narges Eslami, Hossein Bannazadeh Baghi
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引用次数: 0

Abstract

Cervical and other anogenital malignancies are largely caused by E6 and E7 oncogenes of high-risk human papillomaviruses (HPVs), which inhibit important tumor suppressors like p53 and pRb when they are persistently activated. The main goal of traditional treatments is to physically or chemically kill cancer cells, but they frequently only offer temporary relief, have serious side effects, and have a high risk of recurrence. Exploring the efficacy and accuracy of CRISPR-Cas9 gene editing in both inducing death in HPV-infected cancer cells and restoring the activity of tumor suppressors is our main goal. In this study, we propose a novel precision oncology strategy that targets and inhibits the detrimental effects of the E6 and E7 oncogenes using the CRISPR-Cas9 gene editing system. In order to do this, we create unique guide RNAs that target the integrated HPV DNA and reactivate p53 and pRb. Reactivation is meant to halt aberrant cell development and restart the cell's natural dying pathways. This review discusses the potential of CRISPR/Cas9 in targeting HPV oncogenes, with a focus on studies that have demonstrated its promise in cancer treatment. Given the absence of a definitive treatment for papillomavirus infection and its subsequent association with various cancers, future clinical trials and experimental investigations appear essential to establish and evaluate the therapeutic potential of CRISPR-based approaches. This approach provides a less invasive alternative to conventional treatments and opens the door to personalized care that considers the genetic makeup of each patient's tumor.

hpv驱动的癌症:迫在眉睫的威胁和CRISPR/Cas9靶向治疗的潜力。
宫颈和其他肛门生殖器恶性肿瘤主要由高危人乳头瘤病毒(hpv)的E6和E7癌基因引起,当p53和pRb等重要肿瘤抑制因子持续激活时,它们会被抑制。传统治疗的主要目标是物理或化学杀死癌细胞,但它们往往只能提供暂时的缓解,有严重的副作用,并且有很高的复发风险。探索CRISPR-Cas9基因编辑在诱导hpv感染的癌细胞死亡和恢复肿瘤抑制因子活性方面的有效性和准确性是我们的主要目标。在这项研究中,我们提出了一种新的精确肿瘤学策略,利用CRISPR-Cas9基因编辑系统靶向并抑制E6和E7癌基因的有害影响。为了做到这一点,我们创造了独特的引导rna,靶向整合的HPV DNA并重新激活p53和pRb。再激活意味着停止异常的细胞发育,重新启动细胞的自然死亡途径。这篇综述讨论了CRISPR/Cas9靶向HPV癌基因的潜力,重点是已经证明其在癌症治疗中的前景的研究。鉴于乳头瘤病毒感染及其随后与各种癌症的关联缺乏明确的治疗方法,未来的临床试验和实验研究似乎对于建立和评估基于crispr的方法的治疗潜力至关重要。这种方法为传统治疗提供了一种侵入性更小的选择,并为考虑每个患者肿瘤的基因组成的个性化护理打开了大门。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Virology Journal
Virology Journal 医学-病毒学
CiteScore
7.40
自引率
2.10%
发文量
186
审稿时长
1 months
期刊介绍: Virology Journal is an open access, peer reviewed journal that considers articles on all aspects of virology, including research on the viruses of animals, plants and microbes. The journal welcomes basic research as well as pre-clinical and clinical studies of novel diagnostic tools, vaccines and anti-viral therapies. The Editorial policy of Virology Journal is to publish all research which is assessed by peer reviewers to be a coherent and sound addition to the scientific literature, and puts less emphasis on interest levels or perceived impact.
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