{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["7(5)"],"submitter":["Ingles-Esteve J"],"pubmed_abstract":["14-3-3σ is frequently lost in human breast cancers by genetic deletion or promoter methylation. We have now investigated the involvement of 14-3-3σ in the termination of NF-κB signal in mammary cells and its putative role in cancer relapse and metastasis. Our results show that 14-3-3σ regulates nuclear export of p65-NF-κB following chronic TNFα stimulation. Restoration of 14-3-3σ in breast cancer cells reduces migration capacity and metastatic abilities in vivo. By microarray analysis, we have identified a genetic signature that responds to TNFα in a 14-3-3σ-dependent manner and significantly associates with different breast and other types of cancer. By interrogating public databases, we have found that over-expression of this signature correlates with poor relapse-free survival in breast cancer patients. Finally, screening of 96 human breast tumors showed that NF-κB activation strictly correlates with the absence of 14-3-3σ and it is significantly associated with worse prognosis in the multivariate analysis. Our findings identify a genetic signature that is important for breast cancer prognosis and for future personalized treatments based on NF-κB targeting."],"journal":["PloS one"],"pagination":["e38347"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3364992"],"repository":["biostudies-literature"],"pubmed_title":["Inhibition of specific NF-κB activity contributes to the tumor suppressor function of 14-3-3σ in breast cancer."],"pmcid":["PMC3364992"],"pubmed_authors":["Albanell J","Espinosa L","Ruiz-Herguido C","Iglesias M","Rovira A","Jene-Sanz A","Ingles-Esteve J","Lopez-Bigas N","Gomis RR","Bigas A","Morales M","Rojo F","Garcia-Carbonell R","Dalmases A"],"additional_accession":[]},"is_claimable":false,"name":"Inhibition of specific NF-κB activity contributes to the tumor suppressor function of 14-3-3σ in breast cancer.","description":"14-3-3σ is frequently lost in human breast cancers by genetic deletion or promoter methylation. We have now investigated the involvement of 14-3-3σ in the termination of NF-κB signal in mammary cells and its putative role in cancer relapse and metastasis. Our results show that 14-3-3σ regulates nuclear export of p65-NF-κB following chronic TNFα stimulation. Restoration of 14-3-3σ in breast cancer cells reduces migration capacity and metastatic abilities in vivo. By microarray analysis, we have identified a genetic signature that responds to TNFα in a 14-3-3σ-dependent manner and significantly associates with different breast and other types of cancer. By interrogating public databases, we have found that over-expression of this signature correlates with poor relapse-free survival in breast cancer patients. Finally, screening of 96 human breast tumors showed that NF-κB activation strictly correlates with the absence of 14-3-3σ and it is significantly associated with worse prognosis in the multivariate analysis. Our findings identify a genetic signature that is important for breast cancer prognosis and for future personalized treatments based on NF-κB targeting.","dates":{"release":"2012-01-01T00:00:00Z","publication":"2012","modification":"2026-04-07T20:09:59.043Z","creation":"2026-04-07T17:26:24.347Z"},"accession":"S-EPMC3364992","cross_references":{"pubmed":["22675457"],"doi":["10.1371/journal.pone.0038347"]}}