{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["86"],"submitter":["Kiran S"],"pubmed_abstract":["Pancreatic ductal adenocarcinoma (PDAC) remains highly resistant to therapy, surviving despite hypoxia, oxidative stress, and nutrient deprivation. Redox effector factor-1 (Ref-1) regulates several oncogenic transcription factors (TFs) and is controlled by peroxiredoxins (PRDX). We investigated how Ref-1 inhibition by APX2014, combined with PRDX expression, affects pancreatic cancer cells from multiple patient lines. Silencing or CRISPR/Cas9 knockout of PRDX1-but not PRDX2-6-sensitized PDAC cell lines to APX2014 both in vitro and in vivo without affecting Ref-1's DNA repair function of apurinic/apyrimidinic endonuclease. The combination of PRDX1 loss and APX2014 treatment increased apoptosis and decreased TF activity (NF-κB, HIF-1α) and their downstream targets, TNFAIP2, Survivin, and CA9."],"journal":["Redox biology"],"pagination":["103848"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12445586"],"repository":["biostudies-literature"],"pubmed_title":["The absence of Peroxiredoxin-1 in human pancreatic ductal adenocarcinoma (PDAC) markedly reduces cell survival and tumor growth when coupled with the inhibition of Ref-1 redox signaling."],"pmcid":["PMC12445586"],"pubmed_authors":["Kiran S","Kelley MR","Haiaty S","Peil J","Wireman RS","Fishel ML","Potchanant ES","Cao S","Mitchell DK","Vilseck JZ","Georgiadis MM","Rai R"],"additional_accession":[]},"is_claimable":false,"name":"The absence of Peroxiredoxin-1 in human pancreatic ductal adenocarcinoma (PDAC) markedly reduces cell survival and tumor growth when coupled with the inhibition of Ref-1 redox signaling.","description":"Pancreatic ductal adenocarcinoma (PDAC) remains highly resistant to therapy, surviving despite hypoxia, oxidative stress, and nutrient deprivation. Redox effector factor-1 (Ref-1) regulates several oncogenic transcription factors (TFs) and is controlled by peroxiredoxins (PRDX). We investigated how Ref-1 inhibition by APX2014, combined with PRDX expression, affects pancreatic cancer cells from multiple patient lines. Silencing or CRISPR/Cas9 knockout of PRDX1-but not PRDX2-6-sensitized PDAC cell lines to APX2014 both in vitro and in vivo without affecting Ref-1's DNA repair function of apurinic/apyrimidinic endonuclease. The combination of PRDX1 loss and APX2014 treatment increased apoptosis and decreased TF activity (NF-κB, HIF-1α) and their downstream targets, TNFAIP2, Survivin, and CA9.","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Sep","modification":"2026-06-03T14:30:27.152Z","creation":"2026-04-28T03:11:42.384Z"},"accession":"S-EPMC12445586","cross_references":{"pubmed":["40902319"],"doi":["10.1016/j.redox.2025.103848"]}}