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Functional genomics of HDAC class-I specific inhbitor 4SC-202 in pancreatic cell lines

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE90112 | GEO | 2017/03/14

SECONDARY ACCESSION(S): PRJNA354415

REPOSITORIES: GEO

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Functional genomics of HDAC class-I specific inhbitor 4SC-202 in pancreatic cell lines [ChIP-seq]

Project description:We have utilized a HDAC class-I specific inhbitor 4SC-202 and revealed a potential involvement of BRD4 and MYC in regulating the expression of induced genes in response to 4SC-202 treatment.

2017-03-14 | GSE90110 | GEO

Functional genomics of HDAC class-I specific inhbitor 4SC-202 in pancreatic cell lines [RNA-seq]

Project description:We examined transcriptome-wide effects of 4SC-202 in L3.6, BXPC3 and PANC1 cells as well as its effect on TGFβ signaling

2017-03-14 | GSE90111 | GEO

Functional genomics of HDAC class-I specific inhbitor 4SC-202 in pancreatic cell lines

Project description:Functional genomics of HDAC class-I specific inhbitor 4SC-202 in pancreatic cell lines

| PRJNA354415 | ENA

Evaluation of the Therapeutic Potential of the Novel Isotype Specific HDAC Inhibitor 4SC-202 in Urothelial Carcinoma Cell Lines.

Project description:BackgroundTargeting of class I histone deacetylases (HDACs) exerts antineoplastic actions in various cancer types by modulation of transcription, upregulation of tumor suppressors, induction of cell cycle arrest, replication stress and promotion of apoptosis. Class I HDACs are often deregulated in urothelial cancer. 4SC-202, a novel oral benzamide type HDAC inhibitor (HDACi) specific for class I HDACs HDAC1, HDAC2 and HDAC3 and the histone demethylase LSD1, shows substantial anti-tumor activity in a broad range of cancer cell lines and xenograft tumor models.AimThe aim of this study was to investigate the therapeutic potential of 4SC-202 in urothelial carcinoma (UC) cell lines.MethodsWe determined dose response curves of 4SC-202 by MTT assay in seven UC cell lines with distinct HDAC1, HDAC2 and HDAC3 expression profiles. Cellular effects were further analyzed in VM-CUB1 and UM-UC-3 cells by colony forming assay, caspase-3/7 assay, flow cytometry, senescence assay, LDH release assay, and immunofluorescence staining. Response markers were followed by quantitative real-time PCR and western blotting. Treatment with the class I HDAC specific inhibitor SAHA (vorinostat) served as a general control.Results4SC-202 significantly reduced proliferation of all epithelial and mesenchymal UC cell lines (IC50 0.15-0.51 μM), inhibited clonogenic growth and induced caspase activity. Flow cytometry revealed increased G2/M and subG1 fractions in VM-CUB1 and UM-UC-3 cells. Both effects were stronger than with SAHA treatment.ConclusionSpecific pharmacological inhibition of class I HDACs by 4SC-202 impairs UC cell viability, inducing cell cycle disturbances and cell death. Combined inhibition of HDAC1, HDAC2 and HDAC3 seems to be a promising treatment strategy for UC.

| S-EPMC5153417 | biostudies-literature

Functional Genomics Identifies Metabolic Vulnerabilities in Pancreatic Cancer