{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ellison M"],"funding":["NIH/NCI","NIMHD NIH HHS","National Cancer Institute","DOD Peer Reviewed Cancer Research Program","NCI NIH HHS","National Institute of General Medical Sciences","NIGMS NIH HHS"],"pagination":["15"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6986021"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["18(1)"],"pubmed_abstract":["<h4>Background</h4>We have previously shown that the zinc finger transcription repressor SNAI2 (SLUG) represses tumor suppressor BRCA2-expression in non-dividing cells by binding to the E2-box upstream of the transcription start site. However, it is unclear how proliferating breast cancer (BC) cells that has higher oxidation state, overcome this repression. In this study, we provide insight into the mechanism of de-silencing of BRCA2 gene expression by PRDX5A, which is the longest member of the peroxiredoxin5 family, in proliferating breast cancer cells.<h4>Methods</h4>We used cell synchronization and DNA affinity pulldown to analyze PRDX5A binding to the BRCA2 silencer. We used oxidative stress and microRNA (miRNA) treatments to study nuclear localization of PRDX5A and its impact on BRCA2"],"journal":["Cell communication and signaling : CCS"],"pubmed_title":["The role of the redox/miR-6855-3p/PRDX5A axis in reversing SLUG-mediated BRCA2 silencing in breast cancer cells."],"pmcid":["PMC6986021"],"funding_grant_id":["BC050641","1U54RR026140","2U54MD007586-32","BC990678","BC103645","1R21CA181920 01","S21 MD000104"],"pubmed_authors":["Chaudhuri G","Chaudhuri M","Ellison M","Mittal M","Misra S"],"additional_accession":[]},"is_claimable":false,"name":"The role of the redox/miR-6855-3p/PRDX5A axis in reversing SLUG-mediated BRCA2 silencing in breast cancer cells.","description":"<h4>Background</h4>We have previously shown that the zinc finger transcription repressor SNAI2 (SLUG) represses tumor suppressor BRCA2-expression in non-dividing cells by binding to the E2-box upstream of the transcription start site. However, it is unclear how proliferating breast cancer (BC) cells that has higher oxidation state, overcome this repression. In this study, we provide insight into the mechanism of de-silencing of BRCA2 gene expression by PRDX5A, which is the longest member of the peroxiredoxin5 family, in proliferating breast cancer cells.<h4>Methods</h4>We used cell synchronization and DNA affinity pulldown to analyze PRDX5A binding to the BRCA2 silencer. We used oxidative stress and microRNA (miRNA) treatments to study nuclear localization of PRDX5A and its impact on BRCA2","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Jan","modification":"2026-05-07T00:42:24.901Z","creation":"2020-05-22T08:35:42Z"},"accession":"S-EPMC6986021","cross_references":{"pubmed":["31987042"],"doi":["10.1186/s12964-019-0493-5"]}}