<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>23(1)</volume><submitter>Ma L</submitter><pubmed_abstract>Acute myeloid leukemia (AML) is a highly cancerous and aggressive hematologic disease with elevated levels of drug resistance and relapse resulting in high mortality. Recently, bromodomains and extra-terminal (BET) protein inhibitors have been extensively researched in hematological tumors as potential anticancer agents. MZ1 is a novel BET inhibitor that mediates selective proteins degradation and suppression of tumor growth through proteolysis-targeting chimeras (PROTAC) technology. Accordingly, this study aimed to investigate the role and therapeutic potential of MZ1 in AML. In this study, we first identified that AML patients with high BRD4 expression had poor overall survival than those with low expression group. MZ1 inhibited AML cell growth and induced apoptosis and cycle arrest in v</pubmed_abstract><journal>Cancer biology &amp; therapy</journal><pagination>1-15</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9543111</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>BRD4 PROTAC degrader MZ1 exerts anticancer effects in acute myeloid leukemia by targeting c-Myc and ANP32B genes.</pubmed_title><pmcid>PMC9543111</pmcid><pubmed_authors>Hu S</pubmed_authors><pubmed_authors>Ma L</pubmed_authors><pubmed_authors>Zhang K</pubmed_authors><pubmed_authors>Fang F</pubmed_authors><pubmed_authors>Chu X</pubmed_authors><pubmed_authors>Ling J</pubmed_authors><pubmed_authors>Wan X</pubmed_authors><pubmed_authors>Yu J</pubmed_authors><pubmed_authors>Wang J</pubmed_authors><pubmed_authors>Li X</pubmed_authors><pubmed_authors>Lu L</pubmed_authors><pubmed_authors>Pan J</pubmed_authors><pubmed_authors>Li Z</pubmed_authors><pubmed_authors>Sang X</pubmed_authors><pubmed_authors>Zhang Z</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Tao Y</pubmed_authors><pubmed_authors>Tian Y</pubmed_authors><pubmed_authors>Lu J</pubmed_authors><pubmed_authors>Wu S</pubmed_authors><pubmed_authors>Chen Y</pubmed_authors><pubmed_authors>Zhuo R</pubmed_authors></additional><is_claimable>false</is_claimable><name>BRD4 PROTAC degrader MZ1 exerts anticancer effects in acute myeloid leukemia by targeting c-Myc and ANP32B genes.</name><description>Acute myeloid leukemia (AML) is a highly cancerous and aggressive hematologic disease with elevated levels of drug resistance and relapse resulting in high mortality. Recently, bromodomains and extra-terminal (BET) protein inhibitors have been extensively researched in hematological tumors as potential anticancer agents. MZ1 is a novel BET inhibitor that mediates selective proteins degradation and suppression of tumor growth through proteolysis-targeting chimeras (PROTAC) technology. Accordingly, this study aimed to investigate the role and therapeutic potential of MZ1 in AML. In this study, we first identified that AML patients with high BRD4 expression had poor overall survival than those with low expression group. MZ1 inhibited AML cell growth and induced apoptosis and cycle arrest in v</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Dec</publication><modification>2026-04-08T18:01:26.542Z</modification><creation>2025-02-19T01:28:00.408Z</creation></dates><accession>S-EPMC9543111</accession><cross_references><pubmed>36170346</pubmed><doi>10.1080/15384047.2022.2125748</doi></cross_references></HashMap>