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Targeting of REST with rationally-designed small-molecule compounds exhibits synergetic therapeutic potential in human glioblastoma cells

ABSTRACT: Targeting of REST with rationally-designed small-molecule compounds exhibits synergetic therapeutic potential in human glioblastoma cells

PROVIDER: PRJNA983731 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24915409.fastq.gz	Fastqsanger.gz
	SRR24915410.fastq.gz	Fastqsanger.gz
	SRR24915411.fastq.gz	Fastqsanger.gz
	SRR24915412.fastq.gz	Fastqsanger.gz
	SRR24915413.fastq.gz	Fastqsanger.gz

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Targeting of REST with rationally-designed small-molecule compounds exhibits synergetic therapeutic potential in human glioblastoma cells

Project description:To validate role of REST (RE-1 silencing transcription factor) in glioblastoma (GBM) growth, we used CRISPR/Cas9 gene editing to generate REST-null single-cell clonal lines from GBM cell line (T98G) and non-neural HEK293 cells. We then performed gene expression profiling using data obtained from Tag-Seq of 8 cell lines: T98G CRISRP Control and 4 T98G REST-KO clones (C10, F7, G2, D4); HEK293 CRISPR Control and 2 HEK293 REST-KO clones (D10, E6).

2024-03-27 | GSE234912 | GEO

Targeting of REST with rationally-designed small molecule compounds exhibits synergetic therapeutic potential in human glioblastoma cells.

Project description:BackgroundGlioblastoma (GBM) is an aggressive brain cancer associated with poor prognosis, intrinsic heterogeneity, plasticity, and therapy resistance. In some GBMs, cell proliferation is fueled by a transcriptional regulator, repressor element-1 silencing transcription factor (REST).ResultsUsing CRISPR/Cas9, we identified GBM cell lines dependent on REST activity. We developed new small molecule inhibitory compounds targeting small C-terminal domain phosphatase 1 (SCP1) to reduce REST protein level and transcriptional activity in glioblastoma cells. Top leads of the series like GR-28 exhibit potent cytotoxicity, reduce REST protein level, and suppress its transcriptional activity. Upon the loss of REST protein, GBM cells can potentially compensate by rewiring fatty acid metabolism, enabling continued proliferation. Combining REST inhibition with the blockade of this compensatory adaptation using long-chain acyl-CoA synthetase inhibitor Triacsin C demonstrated substantial synergetic potential without inducing hepatotoxicity.ConclusionsOur results highlight the efficacy and selectivity of targeting REST alone or in combination as a therapeutic strategy to combat high-REST GBM.

| S-EPMC11015551 | biostudies-literature

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Project description:A rationally designed JAZ subtype-selective agonist of jasmonate perception

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