Ontology highlight
ABSTRACT:
PROVIDER: PRJNA387217 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Selectively targeting bromodomain and extraterminal proteins for degradation as a novel anti-glioblastoma strategy [ChIP-seq]
| PRJNA387463 | ENA
Project description:Selectively targeting bromodomain and extraterminal proteins for degradation as a novel anti-glioblastoma strategy [RNA-seq]
| PRJNA387467 | ENA
Project description:Selectively targeting bromodomain and extraterminal proteins for degradation as a novel anti-glioblastoma strategy [RNA-seq (time course)
| PRJNA387481 | ENA
Project description:Selectively targeting bromodomain and extraterminal proteins for degradation as a novel anti-glioblastoma strategy NA-seq (time course) May 15, 2018 approved TSV
| PRJNA387477 | ENA
Project description:Remodeling transcription by targeting bromodomain and extraterminal (BET) proteins has emerged as promising anticancer strategy. Here, we identify a novel synergistic interaction of the BET inhibitor JQ1 with the PI3Kα-specific inhibitor BYL719 to trigger mitochondrial apoptosis and to suppress tumor growth in models of rhabdomyosarcoma (RMS). RNA-Seq revealed that JQ1/BYL719 co-treatment shifts the overall balance of BCL-2 family gene expression towards apoptosis and upregulates expression of BMF, BCL2L11 (BIM) and PMAIP1 (NOXA) while downregulating BCL2L1 (BCL-xL).
2020-02-19 | GSE145469 | GEO
Project description:Triple negative breast cancer (TNBC) is an incurable disease with poor prognosis. At this moment, therapeutic options are limited to chemotherapy and no targeted agent has reached the clinical setting. Bromodomain and extraterminal (BET) inhibitors are a new family of compounds that inhibit bromodomain containing proteins affecting the expression of transcription factors (TFs), therefore modifying the expression of relevant oncogenic genes. We decided to performed gene-set enrichment analyses to get insights into the mechanism of action of these compounds. We treated cells with JQ1 and extracted RNA at 12 and 24 hours.
2016-03-23 | E-GEOD-79476 | biostudies-arrayexpress
Project description:Targeting of SMARCA4 bromodomain selectively inhibits leukemic cell proliferation
| PRJNA281224 | ENA
Project description:A systems-level pharmacoproteomics study of a standardized murine model of toll-like receptor (TLR)3-NFκB/RelA innated inflammation in the absence or presence of a highly selective Brd4 (ZL0454) or nonselective Bromodomain and Extraterminal domain inhibitor (JQ1).
2019-07-16 | PXD012060 | Pride
Project description:Bromodomain and extraterminal domain (BET) proteins have emerged as therapeutic targets in multiple cancers, including the most common primary adult brain tumor glioblastoma (GBM). Although several bet inhibitors have entered clinical trials, few are brain penetrant. We have generated UM-002, a novel brain penetrant BET inhibitor that reduces GBM cell proliferation in vitro and in a human cerebral brain organoid model. Since UM-002 is more potent than other BET inhibitors, it could potentially be developed for GBM treatment. Furthermore, UM-002 treatment reduces the expression of cell-cycle related genes in vivo, and reduces the expression of invasion related genes within the non-proliferative cells present in tumors as measured by single cell RNAsequencing. These studies suggest that BET inhibition alters the transcriptional landscape of GBM tumors, which has implications for designing combination therapies. Importantly, they also provide an integrated dataset that combines in vitro and ex vivo studies with in vivo single-cell RNA-sequencing to characterize a novel BET inhibitor in GBM.
2021-12-01 | GSE173146 | GEO
Project description:Hypoxia is negatively associated with glioblastoma patient survival and contributes strongly to tumor resistance. Unfortunately novel anti-angiogenic therapy increases hypoxia and activates survival pathways in tumor cells leading to inevitable tumor relapse. Here we demonstrate that primary glioma cultures and cell lines depend on autophagy to survive severe hypoxia but also at normal oxygen levels. Positive regulators of autophagy are expressed at higher levels in tumor cells and induction in severe hypoxia is more prominent compared to normal brain cells. We demonstrate that autophagy is an essential/critical target for novel treatment in glioblastoma. We show ATG9A is induced by severe hypoxia and could be a novel player of the autophagic response in glioma cells. ATG9A targeting inhibited tumor growth, suggesting an essential role in glioma cell survival in vivo. While autophagy induction was also observed in normal astrocytes, glioma cells displayed a higher sensitivity towards autophagy inhibitors. Importantly, patient-derived cultures exhibited varying sensitivity towards anti-autophagy treatment, where certain cultures were dependent on autophagy already in normoxic conditions. The treatment of tumor bearing mice with the autophagy inhibitor chloroquine significantly increased mice survival, but combination treatment of the agent with bevacizumab did not reveal additive or synergistic effect. The present study demonstrates that inhibition of autophagy using chloroquine as a single agent provides a novel treatment strategy against glioblastoma. It remains to be seen whether autophagy inhibition will improve current standard of care treatment of newly diagnosed glioblastoma patients and whether more specific inhibitors will lead to stronger therapeutic outcome. (Provisional)
2015-11-10 | E-MTAB-3085 | biostudies-arrayexpress