A novel discovery in the field of pancreatic cancer treatment has been unveiled, revealing the epigenetic silencing of BEND4 as a potential synthetic lethal marker for enhancing the efficacy of ATM inhibitors in pancreatic cancer treatment. This research provides an approach to targeting a tumor suppressor gene , BEND4, which is frequently methylated and silenced in pancreatic cancer . The findings are published in the journal Frontiers of Medicine .
The study delves into the role of BEND4 in DNA damage repair and its potential as a therapeutic marker when combined with ATM inhibitor treatment. The investigation was conducted using a comprehensive methodology, including cell line experiments, tissue sample analysis, and in vivo studies. The researchers evaluated the expression and methylation status of BEND4 in various pancreatic cancer cell lines and tissues, finding a significant association between BEND4 methylation and poor tumor differentiation.
Furthermore, BEND4 methylation was identified as an independent poor prognostic marker for patients with pancreatic ductal adenocarcinoma (PDAC). The study demonstrated that BEND4 suppresses cell growth , induces G1/S arrest and apoptosis, and inhibits migration and invasion in PDAC cells. The underlying mechanism involves BEND4's interaction with Ku80, a key player in the non-homologous end joining (NHEJ) pathway, which is a major DNA double-strand break (DSB) repair pathway.
The research showed that BEND4 overexpression enhance.
