Targeting TCA cycle through Cuproptosis confers Synthetic Lethality to ARID1A Deficiency Hepatocellular Carcinoma [ATAC-Seq]
To further explore the mechanisms of  glucose metabolic reprogramming in ARID1A deficiency HCC, we conducted multi-omics profilings in ARID1A deficient and wild type Hep3B cells. Overall design: ATAC-seq was performed to determine chromatin accessibility in ARID1A deficient and wild type Hep3B cells.