{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"submitter":["Kpenu EK"],"funding":["NCI NIH HHS"],"pubmed_abstract":["<h4>Background</h4>Pancreatic ductal adenocarcinoma (PDAC) is a highly deadly cancer with limited treatment options. The base excision repair (BER) pathway, crucial for fixing DNA abasic sites, is driven by apurinic/apyrimidinic endonuclease 1 (APE1). While APE1's redox function has been extensively studied, its endonuclease activity in PDAC homeostasis and therapeutic response remains poorly understood. We created stable, homozygous APE1 endonuclease-reduced PDAC cell lines to examine the effects of impaired BER activity on pancreatic cancer growth, progression, and response to treatment.<h4>Methods</h4>CRISPR/Cas9-mediated editing was used to introduce an E96A mutation into the Pa03C PDAC cell line, generating three clonal mutant cell lines: E96A B1, E96A B4, E96A G8. APE1 expression and"],"journal":["Research square"],"pagination":["rs.3.rs-8197122"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12776480"],"repository":["biostudies-literature"],"pubmed_title":["Targeting APE1 endonuclease activity impairs metastasis and enhances genotoxic therapy response in pancreatic cancer."],"pmcid":["PMC12776480"],"funding_grant_id":["R01 CA282478","R01 CA254110","P30 CA082709","U01 CA274304"],"pubmed_authors":["Kelley MR","Haiaty S","Peil J","Wireman RS","Liu S","Kpenu EK","Gampala S","Sharma A","Mijiti M","Sardar R","Fishel ML","Wan J","Mitchell DK","Georgiadis MM"],"additional_accession":[]},"is_claimable":false,"name":"Targeting APE1 endonuclease activity impairs metastasis and enhances genotoxic therapy response in pancreatic cancer.","description":"<h4>Background</h4>Pancreatic ductal adenocarcinoma (PDAC) is a highly deadly cancer with limited treatment options. The base excision repair (BER) pathway, crucial for fixing DNA abasic sites, is driven by apurinic/apyrimidinic endonuclease 1 (APE1). While APE1's redox function has been extensively studied, its endonuclease activity in PDAC homeostasis and therapeutic response remains poorly understood. We created stable, homozygous APE1 endonuclease-reduced PDAC cell lines to examine the effects of impaired BER activity on pancreatic cancer growth, progression, and response to treatment.<h4>Methods</h4>CRISPR/Cas9-mediated editing was used to introduce an E96A mutation into the Pa03C PDAC cell line, generating three clonal mutant cell lines: E96A B1, E96A B4, E96A G8. APE1 expression and","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Dec","modification":"2026-07-05T03:10:17.967Z","creation":"2026-07-05T03:08:10.845Z"},"accession":"S-EPMC12776480","cross_references":{"pubmed":["41510226"],"doi":["10.21203/rs.3.rs-8197122/v1"]}}