Project description:4 lymphoma cell lines (DOHH2, OCILy10, TMD8 and Toledo) have been treated with MZ1. The transcriptome has been sequenced after 6hrs from the treatment
Project description:We used DNA microarray technology to assess changes in gene expression after treatment of 11 lymphoma cell lines with epigenetic drugs. We identified genes with upregulated expression in treated cell lines and with downregulated expression in B-cell lymphoma patient samples when compared to normal B cells.
Project description:We used DNA microarray technology to assess changes in gene expression after treatment of 11 lymphoma cell lines with epigenetic drugs. We identified genes with upregulated expression in treated cell lines and with downregulated expression in B-cell lymphoma patient samples when compared to normal B cells. Assess changes in gene expression after treatment of 11 lymphoma cell lines with epigenetic drugs (aza and TSA).
Project description:MZ1 is a newly designed pan-BET-targeting PROTAC that binds to target proteins (BET proteins such as BRD2, BRD3, and BRD4) and recruits them to the ubiquitin/protease pathway for selective destruction. However, the role of MZ1 in NB models has yet to be determined. The effect of MZ1 on NB cells was investigated using RNA-seq analysis in this work. MZ1 is a newly designed pan-BET-targeting PROTAC that binds to target proteins (BET proteins such as BRD2, BRD3, and BRD4) and recruits them to the ubiquitin/protease pathway for selective destruction. However, the role of MZ1 in NB models has yet to be determined. The effect of MZ1 on NB cells was investigated using RNA-seq analysis in this work.
Project description:To investigate the function of MZ1 in the regulation of gene expression, we treated U87 cells with control (DMSO) or MZ1, respectively. We then performed gene expression profiling analysis using data obtained from RNA-seq of control and MZ1 treatment.
Project description:Acute lymphoblastic leukemia (ALL) is the most common childhood malignancy. B-cell acute myeloid leukemia (B-ALL) predominates in ALL, with current cure rates of ∼80%. However, the long-term survival rate of patients with early relapse or refractory B-ALL is very low. In recent years, Bromodomains and extra-terminal (BET) protein inhibitors have shown considerable prospect in hematological tumors. MZ1 is a novel BET inhibitor that degrades target proteins and inhibits tumor growth through proteolysis-targeting chimeras (PROTAC) technology. This study shows that MZ1 has cytotoxic effects on 697 (TCF3/PBX1) and RS4;11 (MLL-AF4) B-ALL cell lines representing different molecular subtypes of B-ALL. Furthermore, we observed that MZ1 could promote cell apoptosis, induce cells cycle arrest and inhibit B-ALL cell proliferation by depleting BET protein and downregulating the transcription of CCND3. Collectively, our results indicate that MZ1 might be exploited as a novel therapeutic strategy for the treatment of B-ALL.
Project description:We used CRISPR/Cas9 to intoroduce frame-shifting mutations into the ABCC1 and ABCB1 genes and treated HAP1 WT cells with varying concentrations of the MZ1 PROTAC. To measure the transcriptional response to both genetic and chemical perturbances, we performed RNA-seq and quantified gene expression levels.