<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>8(45)</volume><submitter>Zhou Z</submitter><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&lt;sup>Kip1&lt;/sup> promoter. Moreover, silencing HO-1 gene expression enhanced vorinostat-induced tumor cell apoptosis, prolonged sur</pubmed_abstract><journal>Oncotarget</journal><pagination>78480-78495</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5667976</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Silencing heme oxygenase-1 increases the sensitivity of ABC-DLBCL cells to histone deacetylase inhibitor &lt;i>in vitro&lt;/i> and &lt;i>in vivo&lt;/i>.</pubmed_title><pmcid>PMC5667976</pmcid><pubmed_authors>Zhe N</pubmed_authors><pubmed_authors>Liao Y</pubmed_authors><pubmed_authors>Cheng B</pubmed_authors><pubmed_authors>Hu X</pubmed_authors><pubmed_authors>Liu P</pubmed_authors><pubmed_authors>Li P</pubmed_authors><pubmed_authors>Lin X</pubmed_authors><pubmed_authors>Wang J</pubmed_authors><pubmed_authors>Zhou Z</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Fang Q</pubmed_authors><pubmed_authors>Tang S</pubmed_authors><pubmed_authors>Lu T</pubmed_authors><pubmed_authors>Ren M</pubmed_authors><pubmed_authors>Ma D</pubmed_authors></additional><is_claimable>false</is_claimable><name>Silencing heme oxygenase-1 increases the sensitivity of ABC-DLBCL cells to histone deacetylase inhibitor &lt;i>in vitro&lt;/i> and &lt;i>in vivo&lt;/i>.</name><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&lt;sup>Kip1&lt;/sup> promoter. Moreover, silencing HO-1 gene expression enhanced vorinostat-induced tumor cell apoptosis, prolonged sur</description><dates><release>2017-01-01T00:00:00Z</release><publication>2017 Oct</publication><modification>2026-06-08T03:55:26.447Z</modification><creation>2019-03-27T03:00:44Z</creation></dates><accession>S-EPMC5667976</accession><cross_references><pubmed>29108243</pubmed><doi>10.18632/oncotarget.19652</doi></cross_references></HashMap>