Project description:To explore the molecular mechanisms by which romidepsin potentiates the effect of talazoparib, RNA sequencing analysis of MBL2 cell lines treated with talazoparib, romidepsin, or talazoparib plus romidepsin was performed. 40% of the 2023 genes in combination were from talazoparib, whereas only 5.9% of the genes deregulated during the treatment with the combination of talazoparib plus romidepsin were from the effect of romidepsin. 94 genes were presented in all three treatment groups and included upregulation of Prdm1, Dusp5, and CD74, among others. Analysis of genes responsible for DNA repair, cell cycle arrest and apoptosis demonstrated the contribution of romidepsin to downregulation of DNA repair, the synergistic effect of romidepsin and talazoparib on downregulation of genes of cell cycle leading to cell cycle arrest, and activation of apoptosis by talazoparib predominantly.
Project description:Romidepsin displayed potent antitumor activity in our lenvatinib-resistant PDCs, we wanted to investigate the underlying mechanism of how romidepsin initiated susceptibility to conquer lenvatinib resistance in liver cancer.
Project description:We have optimized the metabolic tagging of newly transcribed RNAs by 4-thiouridine (4sU) to identify newly-transcribed (nascent) circRNAs from human PA1 cells, undifferentiated H9 cells and H9 differentiated FB neurons.
Project description:Tamoxifen enhances romidepsin-induced senescence in pancreatic cancer cells. We compared gene-expression profile among untreated control, romidepsin-treated, tamoxifen-treated, and romidepsin plus tamoxifen-treated Panc1 cells.
Project description:Global gene expression analysis was performed on 8 cancer cell lines after treatment with romidepsin for 6h, or 6h treatment followed by 12 h incubation with drug free medium. The cell lines were selected based on their response spectrum to romidepsin, and included HUT78, LOXIMVI, M14, A549, MDA231, ACHN, MiaPaca2 and PC3. Differentially expressed genes (DEG) included genes involved in DNA damage repair (DDR) pathways. The Affymetrix Human Genome U133 Plus 2.0 platform was used for the gene expression profiling.
Project description:In this study, we demonstrated the synergistic effect of the mechlorethamine-romidepsin combination in cutaneous T cell lymphoma cell lines and CD4+ T cells derived from patients with Sezary Syndrome. We identify the signaling pathways specifically perturbed under treatment with mechlorethamine-romidepsin combination.
Project description:ChIP-seq. analysis of TCam-2 16 h after 10 nanomolar Romidepsin application. DMSO treated cells were used as controls. For ChIP, an antibody against histone H3 pan-acetylation was used. These data are part of the article 'The Histone Deacetylase Inhibitor Romidepsin Efficiently Targets Cisplatin-resistant Germ Cell Cancer Cells via Downregulation of the SWI/SNF-Complex Member ARID1A' (Nettersheim et al., 2016). TCam-2 cells treated for 16h with romidepsin or the solvent were fixed by formaldehyde solution and further processed by Active Motif, including DNA shearing by sonication, chromatin-immunoprecipitaion, library generation and sequencing (NextSeq 500, Illumina). Pooled input DNA of each sample including spike-in Drosophila DNA was used as controls and for normalization. The 75-nt sequence reads were mapped against the genome using BWA algorithm. Duplicate reads were removed. Only peaks that align with no more than 2 mismatches and map uniquely to the genome were used for further analysis. Intervals / peaks were identified by the MACS peak finding algorithm (cutoff p-value 1x10-7) including ENCODE blacklist filtering