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MARS-seq on SU-DIPG13 cells treated Sulfopin/Vorinostat/Sulfopin+Vorinostat or DMSO

ABSTRACT: MARS-seq on SU-DIPG13 cells treated Sulfopin/Vorinostat/Sulfopin+Vorinostat or DMSO

PROVIDER: PRJNA915084 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22868800.fastq.gz	Fastqsanger.gz
	SRR22868801.fastq.gz	Fastqsanger.gz
	SRR22868802.fastq.gz	Fastqsanger.gz
	SRR22868803.fastq.gz	Fastqsanger.gz
	SRR22868804.fastq.gz	Fastqsanger.gz

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Cut&Run and MARS-seq on SU-DIPG13 cells treated Sulfopin/Vorinostat/Sulfopin+Vorinostat or DMSO

Project description:Cut&Run and MARS-seq on SU-DIPG13 cells treated Sulfopin/Vorinostat/Sulfopin+Vorinostat or DMSO

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Cut&Run SU-DIPG13 cells treated Sulfopin/Vorinostat/Sulfopin+Vorinostat or DMSO

Project description:Cut&Run SU-DIPG13 cells treated Sulfopin/Vorinostat/Sulfopin+Vorinostat or DMSO

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MARS-seq on SU-DIPG13 cells treated Sulfopin/Vorinostat/Sulfopin+Vorinostat or DMSO

Project description:Diffuse midline gliomas (DMG) are aggressive pediatric tumors of the central nervous system that are highly resistant to treatments and are inevitably fatal. Lysine to methionine substitution of residue 27 on histone H3 (H3-K27M) is a driver mutation in DMGs, reshaping the epigenetic landscape of these cells to promote tumorigenesis. H3-K27M gliomas are characterized by deregulation of histone acetylation and methylation pathways, as well as the oncogenic MYC pathway. In search of effective treatment, we examined the therapeutic potential of dual targeting of histone deacetylases (HDACs) and MYC in these tumors. Treatment of H3-K27M patient-derived cells with Sulfopin, an inhibitor shown to block MYC-driven tumors in vivo, in combination with the HDAC inhibitor Vorinostat, resulted in substantial decrease in cell viability. Moreover, transcriptome and epigenome profiling revealed synergistic effect of this drug combination in downregulation of prominent oncogenic pathways such as mTOR. Finally, in vivo studies of patient-derived orthotopic xenograft models showed significant tumor size reduction in mice treated with the drug combination. These results highlight the combined treatment of Sulfopin and Vorinostat as a promising therapeutic approach for these aggressive tumors.

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Cut&Run SU-DIPG13 cells treated Sulfopin/Vorinostat/Sulfopin+Vorinostat or DMSO

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Cut&Run and MARS-seq on SU-DIPG13 cells treated Sulfopin/Vorinostat/Sulfopin+Vorinostat or DMSO

Project description:This SuperSeries is composed of the SubSeries listed below.

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Transcriptome analysis for vorinostat-treated choriocarcinoma cells

Project description:Choriocarcinoma is one of the rare gynecological malignancies with aggressive behavior. Vorinostat is an approved HDAC inhibitor, and HDACs play important roles in regulating gene expression and modulating various cellular processes. Here, the human choriocarcinoma cell lines (JAR and JEG-3) were treated with 1 μM vorinostat or DMSO for 48 h. Then, total RNA was extracted, and transcriptome analysis was performed.

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Sulfopin, a covalent inhibitor of Pin1, blocks Myc-driven tumors in vivo

Project description:The peptidyl-prolyl isomerase, Pin1, is exploited in cancer to activate oncogenes and inactivate tumor suppressors. However, despite considerable efforts, Pin1 has remained an elusive drug target. Here, we screened an electrophilic fragment library to identify covalent inhibitors targeting Pin1’s active site Cys113, leading to the development of Sulfopin, a nanomolar Pin1 inhibitor. Sulfopin is highly selective, as validated by two independent chemoproteomics methods, achieves potent cellular and in vivo target engagement, and phenocopies Pin1 genetic knockout. Pin1 inhibition had only a modest effect on cancer cell line viability. Still, Sulfopin induced downregulation of c-Myc target genes, reduced tumor progression and conferred survival benefit in murine and zebrafish models of MYCN-driven neuroblastoma, and in a murine model of pancreatic cancer. Our results demonstrate that Sulfopin is a suitable chemical probe for assessing Pin1-dependent pharmacology in cells and in vivo, and that Pin1 warrants further investigation as a potential cancer drug target.

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Comprehensive gene expression profiles of NK cell neoplasms identify vorinostat as an effective drug candidate

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