{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["8(45)"],"submitter":["Zhou Z"],"pubmed_abstract":["Heme oxygenase-1 (HO-1) can promote tumor growth and reinforce the resistance of diffuse large B-cell lymphoma (DLBCL) cells to chemotherapeutic drug vincristine. We herein found that HO-1 protein expression was higher in high-risk DLBCL patients than in low-risk ones. Silencing HO-1 gene expression resisted vorinostat-induced apoptosis and arrested cell cycle in the G0/G1 phase of LY-10 cells. Western blot, co-immunoprecipitation and chromatin immunoprecipitation assays confirmed that the possible mechanisms may be increased cleaved caspase-3 protein expression, decreased phospho-histone deacetylase 3 protein expression, and activated histone acetylation of P27<sup>Kip1</sup> promoter. Moreover, silencing HO-1 gene expression enhanced vorinostat-induced tumor cell apoptosis, prolonged sur"],"journal":["Oncotarget"],"pagination":["78480-78495"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5667976"],"repository":["biostudies-literature"],"pubmed_title":["Silencing heme oxygenase-1 increases the sensitivity of ABC-DLBCL cells to histone deacetylase inhibitor <i>in vitro</i> and <i>in vivo</i>."],"pmcid":["PMC5667976"],"pubmed_authors":["Zhe N","Liao Y","Cheng B","Hu X","Liu P","Li P","Lin X","Wang J","Zhou Z","Zhang Y","Fang Q","Tang S","Lu T","Ren M","Ma D"],"additional_accession":[]},"is_claimable":false,"name":"Silencing heme oxygenase-1 increases the sensitivity of ABC-DLBCL cells to histone deacetylase inhibitor <i>in vitro</i> and <i>in vivo</i>.","description":"Heme oxygenase-1 (HO-1) can promote tumor growth and reinforce the resistance of diffuse large B-cell lymphoma (DLBCL) cells to chemotherapeutic drug vincristine. We herein found that HO-1 protein expression was higher in high-risk DLBCL patients than in low-risk ones. Silencing HO-1 gene expression resisted vorinostat-induced apoptosis and arrested cell cycle in the G0/G1 phase of LY-10 cells. Western blot, co-immunoprecipitation and chromatin immunoprecipitation assays confirmed that the possible mechanisms may be increased cleaved caspase-3 protein expression, decreased phospho-histone deacetylase 3 protein expression, and activated histone acetylation of P27<sup>Kip1</sup> promoter. Moreover, silencing HO-1 gene expression enhanced vorinostat-induced tumor cell apoptosis, prolonged sur","dates":{"release":"2017-01-01T00:00:00Z","publication":"2017 Oct","modification":"2026-06-08T03:55:26.447Z","creation":"2019-03-27T03:00:44Z"},"accession":"S-EPMC5667976","cross_references":{"pubmed":["29108243"],"doi":["10.18632/oncotarget.19652"]}}