{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wang Z"],"funding":["National Natural Science Foundation of China"],"pagination":["738"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7483467"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11(9)"],"pubmed_abstract":["Histone deacetylase 7 (HDAC7), a member of class IIa HDACs, has been described to be an important regulator for B cell development and has a potential role in B cell acute lymphoblastic leukemia (B-ALL). CC1007, a BML-210 analog, is designed to indirectly inhibit class IIa HDACs by binding to myocyte enhancer factor-2 (MEF2) and blocking the recruitment of class IIa HDACs to MEF2-targeted genes to enhance the expression of these targets. In this study, we investigated the anticancer effects of CC1007 in breakpoint cluster region-Abelson 1 fusion gene-negative (BCR-ABL1<sup>-</sup>) pre-B-ALL cell lines and primary patient-derived BCR-ABL1<sup>-</sup> pre-B-ALL cells. CC1007 had obvious antileukemic activity toward pre-B-ALL cells in vitro and in vivo; it also significantly prolonged median"],"journal":["Cell death & disease"],"pubmed_title":["A small molecular compound CC1007 induces cross-lineage differentiation by inhibiting HDAC7 expression and HDAC7/MEF2C interaction in BCR-ABL1<sup>-</sup> pre-B-ALL."],"pmcid":["PMC7483467"],"funding_grant_id":["81500171","81600183","81470323"],"pubmed_authors":["Zhang G","Chen L","Liu S","Li R","Deng M","Cheng Z","Peng H","Zhang Y","Hu G","Chen Y","Luo Y","Wang Z","Zhu S","Xu Y"],"additional_accession":[]},"is_claimable":false,"name":"A small molecular compound CC1007 induces cross-lineage differentiation by inhibiting HDAC7 expression and HDAC7/MEF2C interaction in BCR-ABL1<sup>-</sup> pre-B-ALL.","description":"Histone deacetylase 7 (HDAC7), a member of class IIa HDACs, has been described to be an important regulator for B cell development and has a potential role in B cell acute lymphoblastic leukemia (B-ALL). CC1007, a BML-210 analog, is designed to indirectly inhibit class IIa HDACs by binding to myocyte enhancer factor-2 (MEF2) and blocking the recruitment of class IIa HDACs to MEF2-targeted genes to enhance the expression of these targets. In this study, we investigated the anticancer effects of CC1007 in breakpoint cluster region-Abelson 1 fusion gene-negative (BCR-ABL1<sup>-</sup>) pre-B-ALL cell lines and primary patient-derived BCR-ABL1<sup>-</sup> pre-B-ALL cells. CC1007 had obvious antileukemic activity toward pre-B-ALL cells in vitro and in vivo; it also significantly prolonged median","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Sep","modification":"2025-04-18T18:31:22.506Z","creation":"2020-09-25T07:03:21Z"},"accession":"S-EPMC7483467","cross_references":{"pubmed":["32913188"],"doi":["10.1038/s41419-020-02949-1"]}}