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Global transcriptional profiling of wild type and LATS1/2 KO CAL27 cells in response to indisulam

ABSTRACT: Global transcriptional profiling of wild type and LATS1/2 KO CAL27 cells in response to indisulam

PROVIDER: PRJNA1117821 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29217307_1.fastq.gz	Fastqsanger.gz
	SRR29217307_2.fastq.gz	Fastqsanger.gz
	SRR29217308_1.fastq.gz	Fastqsanger.gz
	SRR29217308_2.fastq.gz	Fastqsanger.gz
	SRR29217309_1.fastq.gz	Fastqsanger.gz

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Global transcriptional profiling of wild type and LATS1/2 KO CAL27 cells in response to indisulam

Project description:mRNA sequencing of WT and LATS1/2 KO CAL27 cells were treated with indisulam 1 μM for 24hr to profile and characterize dysregulated pathways and alternative splicing in response to indisulam

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Transcriptomic analysis of Panc10.05 cells treated with indisulam

Project description:Indisulam is an abandoned drug that acts as a molecular glue, inducing degradation of splicing factor RBM39 through interaction with CRL4DCAF15. We generated spontaneoulsy indisulam-resistant Panc10.05 cells and studied their response to indisulam.

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Exceptional response of high-risk neuroblastoma to RBM39 degrader Indisulam (ATAC-Seq)

Project description:Indisulam selectively bridges splicing factor RBM39 to DCAF15 for proteasomal degradation. However, clinical trials indicate that patient stratification based upon the mechanism of action of indisulam may be required to achieve the best response. Here we show that neuroblastoma, a MYC-driven cancer characterized by splicing dysregulation, requires RBM39 for survival, expresses high levels of DCAF15 among different solid tumor lineages, and is the most sensitive cancer lineage to indisulam that achieves therapeutic effect by specifically targeting RBM39 in neuroblastoma. Genetic depletion or proteasomal degradation of RBM39 by indisulam induces drastic splicing event changes in neuroblastoma cells. Through specifically targeting RBM39, indisulam induces exceptional tumor response in multiple high-risk neuroblastoma models. Collectively we demonstrate that high RBM39 dependency and high-level expression of DCAF15 provide indisulam a more efficacious therapeutic window to treating high-risk neuroblastoma.

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Exceptional response of high-risk neuroblastoma to RBM39 degrader Indisulam (RNA-Seq)

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Project description:For the first time, we investigated the role of TCF4 in CAL27 sphere cells.

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Transcriptomic expression of A549 cells treated with indisulam and sphinx 31

Project description:Indisulam is an abandoned drug that acts as a molecular glue, inducing degradation of splicing factor RBM39 through interaction with CRL4DCAF15. We combined indisulam with sphinx 31 (a splicing factor inhibitor) and evaluated their combined activity in inducing splicing errors.

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Transcriptomic expression of A549 and SUM159 cells treated with palbociclib and indisulam

Project description:Indisulam is a molecular glue targeting a splicing factor RBM39 for degradation. To assess splicing errors when treating the cells with indisulam, palbociclib and the combination we perform RNA sequencing and analyze splicing errors.

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Indisulam targets RNA splicing and metabolism to serve as a novel therapeutic strategy for high risk neuroblastoma

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