增加病例负荷:Cas9诱导的无根据p53信号。

Molecular & cellular oncology Pub Date : 2020-07-14 eCollection Date: 2020-01-01 DOI:10.1080/23723556.2020.1789419
Veronica Rendo, Oana M Enache, Uri Ben-David
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引用次数: 0

摘要

我们研究了人类癌细胞系中聚集规则间隔短回文重复(CRISPR)相关蛋白9 (Cas9)表达的遗传和转录变化。对于具有野生型肿瘤蛋白TP53(最著名的是p53)的细胞系子集,我们检测了Cas9引入后p53通路激活,DNA损伤积累和新出现的p53失活突变。我们讨论了我们的发现在基础研究和转化研究中的潜在意义。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Adding to the CASeload: unwarranted p53 signaling induced by Cas9.

We investigated the genetic and transcriptional changes associated with Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) associated protein 9 (Cas9) expression in human cancer cell lines. For a subset of cell lines with a wild-type tumor protein TP53 (best known as p53), we detected p53 pathway activation, DNA damage accumulation and emerging p53-inactivating mutations following Cas9 introduction. We discuss the potential implications of our findings in basic and translational research.

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