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基因修饰使用CRISPR-dCas9-dnmt3a系统作为治疗质瘤的治疗方法

Farbod Taghavi Rad¹, Saied Ghorbian¹, Bahar Naghavi Gargari²

¹Department of Molecular Genetics, Ahar Branch, Islamic Azad University, Ahar, Iran.

Iranian journal of pharmaceutical research : IJPR

|December 20, 2023

概括

这项研究表明,CRISPR/Cas9基因编辑有效地降低了人类端粒酶逆转录酶 (hTERT) 表达和质瘤细胞中的端粒酶活性. 这种抑制hTERT和端粒酶活性导致质瘤细胞生长的减少.

科学领域:

生物技术是生物技术.
分子生物学分子生物学
癌症研究癌症研究

背景情况:

异常的DNA甲基化与包括癌症在内的各种疾病有关.
克里斯普尔/卡斯9基因编辑技术提供了一种精确且具有成本效益的方法来准和纠正甲基化.
端粒酶由hTERT基因编码,对癌细胞生存至关重要.

研究的目的:

评估CRISPR/Cas9在向hTERT基因中的有效性.
通过向hTERT,评估CRISPR/Cas9作为治疗质瘤癌细胞的潜力.

主要方法:

使用EF1a-hsaCas9-U6-gRNA载体转移U87质瘤细胞.
使用聚烯度优化了转化效率.
分析了hTERT表达,端粒酶活性和促进物甲基化,使用实时PCR,流细胞计,西部斑点和HRM分析.
感染细胞的亡率通过流细胞计测量.

主要成果:

与gRNA一起的CRISPR/Cas9显著提高了转染效率.
在转染的U87细胞中,hTERT表达和端粒酶活性降低.
感染CRISPR/Cas9增加了U87细胞的亡.

结论:

开发的CRISPR/Cas9系统有效地降低了hTERT表达和端粒酶活性.
这种减少抑制了质瘤细胞的生长,这表明了质瘤的潜在治疗策略.

关键词:

这就是CRISPR/Cas9的作用.质瘤是一种质瘤.泰隆玛酶的使用方法 hTERT 基因基因基因

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