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Chromatin accessibility and transcriptomic responses to HDAC inhibitors in TP53 mutated patient-derived colon cancer organoids

ABSTRACT: Chromatin accessibility and transcriptomic responses to HDAC inhibitors in TP53 mutated patient-derived colon cancer organoids

PROVIDER: PRJNA1031172 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26481270_1.fastq.gz	Fastqsanger.gz
	SRR26481270_2.fastq.gz	Fastqsanger.gz
	SRR26481271_1.fastq.gz	Fastqsanger.gz
	SRR26481271_2.fastq.gz	Fastqsanger.gz
	SRR26481272_1.fastq.gz	Fastqsanger.gz

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Chromatin accessibility and transcriptomic responses to HDAC inhibitors in TP53 mutated patient-derived colon cancer organoids [RNA-seq]

Project description:Chromatin accessibility and transcriptomic responses to HDAC inhibitors in TP53 mutated patient-derived colon cancer organoids [RNA-seq]

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Chromatin accessibility and transcriptomic responses to HDAC inhibitors in TP53 mutated patient-derived colon cancer organoids [ATAC-seq]

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Chromatin accessibility and transcriptomic responses to HDAC inhibitors in TP53 mutated patient-derived colon cancer organoids [RNA-seq]

Project description:Here we present the generation and characterization of patient-derived organoids (PDOs) from colorectal cancer patients. Two PDOs derived from patients with TP53 mutations were tested with two different HDACIs (SAHA and NKL54). Induction of cell death, transcriptome, and chromatin accessibility changes were analyzed. HDACIs promote the upregulation of low expressed genes and suppress the expression of highly expressed genes. A similar differential effect is also observed at the level of chromatin accessibility. Only SAHA is a potent inducer of cell death. The induction of apoptosis is characterized by the upregulation of BH3-only genes (especially BIK and BMF). Up-regulation of BIK is associated with increased accessibility in an intronic region. SAHA, but not NKL54, also causes downregulation of BCL2L1 and decreases chromatin accessibility in three distinct regions of the BCL2L1 locus. Both inhibitors upregulate the expression of innate immunity genes and members of the MHC family. In conclusion, our studies explain the mechanisms of action of SAHA and cast doubt on the use of NKL54 as a single agent for efficient apoptosis induction.

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Project description:Tumor protein 53 (TP53)-mutated acute myeloid leukemia (AML) is characterized by poor outcomes and the quick development of treatment resistance. Here, we report that simultaneous inhibition of cyclin-dependent kinases (CDKs) and histone deacetylases (HDACs) with dinaciclib and CAY10603, respectively, eliminates the therapeutic response gap between TP53-mutant and TP53 wild-type AML. Biochemical profiling showed that CAY10603 is not only HDAC6-selective but also exhibits pan-HDAC activity similar to suberoylanilide hydroxamic acid, enabling dual targeting of transcriptional and cell cycle pathways. Across parental wild-type lines and isogenic TP53 mutants, the combination consistently suppressed clonogenic growth, induced caspase-dependent apoptosis, and downregulated key regulators such as CDK2, CDK4/6, and their cyclins, while restoring the CDK inhibitor CDKN1A/p21. In an orthotopic NSG mouse model, dinaciclib + CAY10603 significantly reduced leukemia burden and extended survival without adverse toxicity. By “normalizing” TP53-mutant AML to respond like its wild-type counterpart, this pan-HDAC/multi-CDK blockade offers a TP53-agnostic therapeutic option and warrants clinical evaluation as a strategy that remains effective regardless of baseline allelic status.

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Chromatin accessibility and transcriptomic responses to HDAC inhibitors in TP53 mutated patient-derived colon cancer organoids

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

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