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Epigenetic silencing of BEND4,a novel DNA damage repair gene,is a synthetic lethal marker for ATM inhibitor in pancreatic cancer

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Frontiers of Medicine 2024年第4期18卷 721-734页

作者： Yuanxin Yao Honghui Lv Meiying Zhang Yuan Li James G.Herman Malcolm V.Brock Aiai Gao Qian Wang Francois Fuks Lirong Zhang Mingzhou Guo Department of Gastroenterology and Hepatology the First Medical CenterChinese PLA General HospitalBeijing100853China Department of Pharmacology School of Basic Medical SciencesZhengzhou UniversityZhengzhou450001China Henan Institute of Advanced Technology Zhengzhou UniversityZhengzhou450001China UPMC Hillman Cancer Center University of Pittsburgh Medical CenterPittsburghPA15213USA Department of surgery School of MedicineJohns Hopkins School of MedicineBaltimoreMD21287USA Laboratory of Cancer Epigenetics Faculty of MedicineULB-Cancer Research Center(U-CRC)Universite Libre de Bruxelles(ULB)Brussels1070Belgium National Key Laboratory of Kidney Diseases the First Medical CenterChinese PLA General HospitalBeijing100853China

Synthetic lethality is a novel model for cancer *** understand the function and mechanism of BEN domain-containing protein 4(BEND4)in pancreatic cancer,eight cell lines and a total of 492 cases of pancreatic neoplasia samples were included in this ***-specific polymerase chain reaction,CRISPR/Cas9,immunoprecipitation assay,comet assay,and xenograft mouse model were ***4 is a new member of the BEN domain *** expression of BEND4 is regulated by promoter region *** is methylated in 58.1%(176/303)of pancreatic ductal adenocarcinoma(PDAC),33.3%(14/42)of intraductal papillary mucinous neoplasm,31.0%(13/42)of pancreatic neuroendocrine tumor,14.3%(3/21)of mucinous cystic neoplasm,4.3%(2/47)of solid pseudopapillary neoplasm,and 2.7%(1/37)of serous cystic ***4 methylation is significantly associated with late-onset PDAC(>50 years,P<0.01)and tumor differentiation(P<0.0001),and methylation of BEND4 is an independent poor prognostic marker(P<0.01)in ***,BEND4 plays tumor-suppressive roles in vitro and in ***,BEND4 involves non-homologous end joining signaling by interacting with Ku80 and promotes DNA damage *** of BEND4 increased the sensitivity of PDAC cells to ATM ***,the present study revealed an uncharacterized tumor suppressor BEND4 and indicated that methylation of BEND4 may serve as a potential synthetic lethal marker for ATM inhibitor in PDAC treatment.

关键词： BEND4 DNA methylation synthetic lethality nhej pathway

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