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Development and characterization of vorinostat-resistant cutaneous T cell lymphoma cells

ABSTRACT: We demonstrate that vorinostat-resistant HuT78VR exhibits enhanced invasion characteristics and activation of MAPK signaling.

ORGANISM(S): Homo sapiens

PROVIDER: GSE165261 | GEO | 2021/01/22

REPOSITORIES: GEO

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Development and characterization of vorinostat-resistant cutaneous T cell lymphoma cells

Project description:Development and characterization of vorinostat-resistant cutaneous T cell lymphoma cells

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RNA-seq analysis of vorinostat-resistant HCT116 cells following gene knockdown of potential vorinostat-resistance candidate genes

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RNA-seq analysis of vorinostat-resistant HCT116 cells following gene knockdown of potential vorinostat-resistance candidate genes

Project description:Potential vorinostat-resistance candidate genes were identified using RNA interference screening in vorinostat-resistant HCT116 cells (HCT116-VR) using a synthetic lethal approach. In order to understand the mechanisms by which these genes contributed to vorinostat response, transcriptomic analysis was conducted on HCT116-VR cells and those with siRNA-mediated knockdown of each of the vorinostat resistance candidate genes. There are 45 samples in total, from triplicate independent biological experiments of 15 samples each. The negative control to which all gene knockdowns are compared is the mock transfection control (mock).

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RNA-seq analysis of vorinostat-resistant HCT116 cells following gene knockdown of GLI1 or PSMD13 with or without vorinostat treatment

Project description:Transcriptome analysis was conducted on vorinostat resistant HCT116 cells (HCT116-VR) upon knockdown of potential vorinostat resistance candidate genes in the presence and absence of vorinostat. Potential vorinostat resistance candidate genes chosen for this study were GLI1 and PSMD13, which were identified through a genome-wide synthetic lethal RNA interference screen. To understand the transcriptional events underpinning the effect of GLI1 and PSMD13 knockdown (sensitisation to vorinostat-induced apoptosis), cells were first subjected to gene knockdown, then to treatment with vorinsotat or the solvent control. Two timepoints for drug treatment were assessed: a timepoint before induction of apoptosis (4hrs for siGLI1 and 8hrs for siPSMD13) and a timepoint when apoptosis could be detected (8hrs for siGLI1 and 12hrs for siPSMD13). There are 42 samples in total, from triplicate independent biological experiments of 14 samples each.

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Single-cell profiling of cutaneous T-cell lymphoma after treatment with vorinostat and photophoresis.

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Gene expression profiles of Hodgkin’s lymphoma cells after treatment with vorinostat

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