ARID1A-deficient Bladder Cancer is Dependent on PI3K Signaling, and can be Targeted via EZH2 and/or PI3K Pharmacologic Inhibition: Therapeutic Implications

ARID1A-mutant bladder cancer is dependent on PI3K signaling and is sensitive to EZH2 and/or PI3K inhibition. Clinical trials in molecularly selected patients should be considered. Overall design: Cleavage Under Targets & Release Using Nuclease of RT112 cells in triplicate for ARID1A and H3K4me3

ARID1A突变型膀胱癌（ARID1A-mutant bladder cancer）依赖磷脂酰肌醇3-激酶（PI3K）信号通路，且对zeste同源物2增强子（EZH2）及/或PI3K抑制剂敏感，应考虑针对经分子筛选的患者开展相关临床试验。整体实验设计：针对ARID1A与组蛋白H3第4位赖氨酸三甲基化（H3K4me3）靶标，对RT112细胞进行靶标核酸酶切割与释放测序（Cleavage Under Targets & Release Using Nuclease，CUT&RUN）实验，每组设置三次生物学重复。