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Targeting super-enhancer-driven oncogenic transcription by CDK7 inhibition in anaplastic thyroid cancer [ChIP-Seq]

ABSTRACT: Targeting super-enhancer-driven oncogenic transcription by CDK7 inhibition in anaplastic thyroid cancer [ChIP-Seq]

PROVIDER: PRJNA491865 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7876840.fastq.gz	Fastqsanger.gz
	SRR7876841.fastq.gz	Fastqsanger.gz
	SRR7876838.fastq.gz	Fastqsanger.gz
	SRR7876839.fastq.gz	Fastqsanger.gz

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Targeting super-enhancer-driven oncogenic transcription by CDK7 inhibition in anaplastic thyroid cancer

Project description:Anaplastic thyroid carcinoma (ATC) is one of the most aggressive malignancy and accounts for the majority of thyroid cancer-related deaths. Despite intensive research, there remains no effective treatment for patients with ATC. Here, we identify THZ1, a covalent inhibitor of cyclin-dependent kinase 7 (CDK7), as a potent anti-ATC compound by high-throughput chemical screening. ATC cells, but not papillary thyroid cancer (PTC) cells, are exceptionally sensitive to CDK7 inhibition. Analyzing both gene expression profiles and super enhancer (SE) features reveals that the SE-mediated oncogenic transcriptional amplification renders the vulnerability of ATC cells to THZ1 treatment. Combining this integrative analysis with functional assays discovers a number of novel cancer genes of ATC, including PPP1R15A, SMG9 and KLF2. Inhibition of PPP1R15A with Guanabenz (GBZ) or Sephin1 greatly suppresses ATC growth. Significantly, the expression level of PPP1R15A is correlated with CDK7 expression in ATC tissue samples. Elevated expression of PPP1R15A and CDK7 are both associated with poor clinical prognosis in ATC patients. Importantly, GBZ or THZ1 treatment sensitizes ATC cells to conventional chemotherapy. Taken together, these findings demonstrate transcriptional addiction in ATC pathobiology and identify CDK7 and PPP1R15A as potential biomarkers and therapeutic targets for ATC.

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Targeting super-enhancer-driven oncogenic transcription by CDK7 inhibition in anaplastic thyroid cancer [RNA-Seq]

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Targeting super-enhancer-driven oncogenic transcription by CDK7 inhibition in anaplastic thyroid cancer

Project description:Targeting super-enhancer-driven oncogenic transcription by CDK7 inhibition in anaplastic thyroid cancer

| PRJNA491858 | ENA

Targeting super-enhancer-driven oncogenic transcription by CDK7 inhibition in anaplastic thyroid cancer [RNA-Seq]

Project description:Targeting super-enhancer-driven oncogenic transcription by CDK7 inhibition in anaplastic thyroid cancer [RNA-Seq]

| PRJNA491864 | ENA

PIAS2b dsRNAi repression kills by mitotic catastrophe anaplastic thyroid and non-thyroid carcinomas, but not normal thyroid or differentiated carcinomas

Project description:The E3 SUMO ligase PIAS2 is expressed at high levels in differentiated papillary thyroid carcinomas but at low levels in anaplastic thyroid carcinomas (ATC), an undifferentiated cancer with very high mortality. Double-stranded RNA–directed RNA interference (dsRNAi) targeting the PIAS2 isoform beta (PIAS2b) inhibits growth of ATC cell lines and patient primary cultures in vitro and orthotopic patient-derived xenografts (oPDX) in vivo, but not of thyroid cell lines or non-anaplastic primary thyroid cultures (differentiated carcinoma, benign lesions, or normal). PIAS2b-dsRNAi also has an anti-cancer effect on other anaplastic human cancers (pancreas, lung, and gastric). Mechanistically, PIAS2b is required for proper mitotic spindle and centrosome assembly, and it is a dosage-sensitive protein in ATC. Strikingly, PIAS2b-dsRNAi induces mitotic catastrophe at prophase. High-throughput proteomics revealed the proteasome (PSMC5) and spindle cytoskeleton as direct targets of PIAS2b SUMOylation at mitotic initiation. PIAS2b-dsRNAi is a promising therapy for ATC and other aggressive anaplastic cancers.

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