Here, we show that the <i>ATMIN</i> gene, which encodes a cofactor required for activation of ATM kinase by replication stress, is located close to FRA16D and is commonly lost in lung adenocarcinoma.
In lung adenocarcinoma (LAC), we also determined the expression of phosphorylated ataxia telangiectasia mutated kinase and ataxia telangiectasia and Rad3-related protein.
SETD2-mutated LUADs exhibited relatively poor recurrence- free survival (RFS) and mutations in STK11 and ATM were associated with poor RFS among KRAS-mutant tumors.
Loss-of-function mutations in the DNA damage response kinase ATM are common in lung adenocarcinoma but directly targeting these with drugs remains challenging.
This study showed that the individuals with ATMrs189037 AA genotype were at an increased risk for lung adenocarcinoma compared with those carrying the GA or GG genotype (adjusted odds ratios (OR) 1.44, 95% confidence interval (CI) 1.02-2.02, P = 0.039).
Taken together, our results demonstrate that emodin-induced reactive oxygen species generation activates an ATM-p53-Bax-dependent signaling pathway, which consequently leads to mitochondria-dependent apoptotic cell death in human lung adenocarcinoma A549 cells.