文章：

CRISPR/Cas9介导的CD73基因敲除对胰腺癌的影响

Impact of CRISPR/Cas9-Mediated CD73 Knockout in Pancreatic Cancer

原文发布日期：3 October 2023

DOI: 10.3390/cancers15194842

类型: Article

开放获取: 是

英文摘要：

Pancreatic cancer is among the cancers with the highest mortality rates. Most of the patients are found to have advanced cancer, losing the chance of surgical treatment, and there is an urgent need to find new treatment methods. Targeted therapy for specific genes that play a key role in cancer is now an important means to improve the survival rate of patients. We determined that CD73 is highly expressed in pancreatic cancer by flow cytometry and qRT-PCR assays combined with bioinformatics techniques. Application of CRISPR/Cas9 technology to knockout CD73 in human and murine cell lines, respectively, revealed that CD73 inactivation inhibited cell growth and migration and induced G1 cell cycle arrest. We also found that CD73 deletion inhibited the ERK/STAT3 pathway and activated the E-cadherin pathway. In addition, a CRISPR/Cas9 protein kinase library screen was performed and identified Pbk, Fastk, Cdk19, Adck5, Trim28, and Pfkp as possible genes regulating CD73.

摘要翻译： 

胰腺癌是死亡率最高的癌症之一。多数患者确诊时已处于晚期，失去了手术治疗的机会，亟需寻找新的治疗方法。针对在癌症中起关键作用的特定基因进行靶向治疗，现已成为提高患者生存率的重要手段。通过流式细胞术和qRT-PCR检测结合生物信息学技术，我们确定CD73在胰腺癌中高表达。应用CRISPR/Cas9技术分别敲除人和小鼠细胞系中的CD73，发现CD73失活可抑制细胞生长和迁移，并诱导G1期细胞周期阻滞。我们还发现CD73缺失抑制了ERK/STAT3通路并激活了E-cadherin通路。此外，通过CRISPR/Cas9蛋白激酶文库筛选，鉴定出Pbk、Fastk、Cdk19、Adck5、Trim28和Pfkp可能是调控CD73的基因。

原文链接：

Impact of CRISPR/Cas9-Mediated CD73 Knockout in Pancreatic Cancer