{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Pervin S"],"funding":["NIA NIH HHS","NCI NIH HHS"],"pagination":["848-58"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3590675"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["108(4)"],"pubmed_abstract":["<h4>Background</h4>Breast cancer, a heterogeneous disease has been broadly classified into oestrogen receptor positive (ER+) or oestrogen receptor negative (ER-) tumour types. Each of these tumours is dependent on specific signalling pathways for their progression. While high levels of survivin, an anti-apoptotic protein, increases aggressive behaviour in ER- breast tumours, oxidative stress (OS) promotes the progression of ER+ breast tumours. Mechanisms and molecular targets by which OS promotes tumourigenesis remain poorly understood.<h4>Results</h4>DETA-NONOate, a nitric oxide (NO)-donor induces OS in breast cancer cell lines by early re-localisation and downregulation of cellular survivin. Using in vivo models of HMLE(HRAS) xenografts and E2-induced breast tumours in ACI rats, we demon"],"journal":["British journal of cancer"],"pubmed_title":["Oxidative stress specifically downregulates survivin to promote breast tumour formation."],"pmcid":["PMC3590675"],"funding_grant_id":["U54 CA143931","SC1 AG033407-01A1","1SC1 CA165865-01A1","SC1 AG049682","SC1 AG033407","SC1 CA165865","U54CA143931"],"pubmed_authors":["Braga M","Parveen M","Chaudhuri G","Urman R","Singh R","Tran L","Pervin S","Li SA"],"additional_accession":[]},"is_claimable":false,"name":"Oxidative stress specifically downregulates survivin to promote breast tumour formation.","description":"<h4>Background</h4>Breast cancer, a heterogeneous disease has been broadly classified into oestrogen receptor positive (ER+) or oestrogen receptor negative (ER-) tumour types. Each of these tumours is dependent on specific signalling pathways for their progression. While high levels of survivin, an anti-apoptotic protein, increases aggressive behaviour in ER- breast tumours, oxidative stress (OS) promotes the progression of ER+ breast tumours. Mechanisms and molecular targets by which OS promotes tumourigenesis remain poorly understood.<h4>Results</h4>DETA-NONOate, a nitric oxide (NO)-donor induces OS in breast cancer cell lines by early re-localisation and downregulation of cellular survivin. Using in vivo models of HMLE(HRAS) xenografts and E2-induced breast tumours in ACI rats, we demon","dates":{"release":"2013-01-01T00:00:00Z","publication":"2013 Mar","modification":"2026-05-01T05:07:09.928Z","creation":"2026-04-07T16:40:24.895Z"},"accession":"S-EPMC3590675","cross_references":{"pubmed":["23403820"],"doi":["10.1038/bjc.2013.40"]}}