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The Loss of an orphan Nuclear Receptor augments Wnt/β-Catenin signaling via epigenetic dysregulation that promotes Sp1 and Myc interactions in Hepatocellular Carcinoma Development [RNA-seq]

ABSTRACT: The Loss of an orphan Nuclear Receptor augments Wnt/β-Catenin signaling via epigenetic dysregulation that promotes Sp1 and Myc interactions in Hepatocellular Carcinoma Development [RNA-seq]

PROVIDER: PRJNA1015728 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26045817.fastq.gz	Fastqsanger.gz
	SRR26045818.fastq.gz	Fastqsanger.gz
	SRR26045819.fastq.gz	Fastqsanger.gz
	SRR26045820.fastq.gz	Fastqsanger.gz
	SRR26045821.fastq.gz	Fastqsanger.gz

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The loss of an orphan nuclear receptor NR2E3 augments Wnt/β-Catenin signaling via epigenetic dysregulation that promotes the Sp1-β catenin-p300 interactions in hepatocellular carcinoma.

Project description:The orphan nuclear receptor NR2E3 (Nuclear receptor subfamily 2 group E, Member 3) is an epigenetic player essential for p53 activation during liver injuries through its modulation of chromatin accessibility. Nonetheless, a precise tumor suppressive and epigenetic role of NR2E3 in hepatocellular carcinoma (HCC) remains unclear. HCC patients expressing low NR2E3 exhibit unfavorable clinical outcomes, aligning with heightened activation of the WNT/β-catenin signaling pathway. The murine HCC models utilizing NR2E3 knockout mice consistently exhibits accelerated liver tumor formation and progression accompanied by enhanced activation of WNT/β-catenin signaling pathway and inactivation of p53 signaling pathway. At cellular level, the loss of NR2E3 increases the acquisition of aggressive cancer cell phenotype and tumorigenicity and upregulates key genes in the WNT/β-catenin pathway with enhanced chromatin accessibility. This event is mediated through increased formation of active transcription complex involving Sp1, β-catenin, and p300, a histone acetyltransferase, on the promoters of target genes. These findings demonstrate that the loss of NR2E3 promotes WNT/β-catenin signaling activation at cellular, organismal, and clinical levels. In summary, NR2E3 is a novel tumor suppressor that maintains epigenetic homeostasis, thereby preventing activation of WNT/β-catenin signaling that promotes HCC formation and progression.

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The loss of an orphan nuclear receptor NR2E3 augments Wnt/β-Catenin signaling via epigenetic dysregulation that promotes the Sp1-β catenin-p300 interactions in hepatocellular carcinoma.

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The Loss of an orphan Nuclear Receptor augments Wnt/β-Catenin signaling via epigenetic dysregulation that promotes Sp1 and Myc interactions in Hepatocellular Carcinoma Development [FAIRE-seq]

Project description:We previously reported that the nuclear receptor NR2E3 activates the tumor suppressor gene p53 by modulating chromatin accessibility. In this study, we further investigated the impact of NR2E3 deficiency on chromatin accessibility. We used FAIRE-seq (Formaldehyde-Assisted Isolation of Regulatory Elements) analysis to find that NR2E3 loss increased chromatin accessibility in genomic regions interacting with various transcription factors, including Sp1. Additionally, NR2E3 loss enhanced chromatin accessibility and expression of crucial genes, such as JAK1 and PPARD, essential for WNT-β-catenin signaling pathway activation by facilitating interactions between Sp1 and Myc transcription factors at their promoters. Gene set enrichment analysis (GSEA) on mouse liver tumor tissues from wild-type and NR2E3 knockout mice confirmed that NR2E3 ablation activated WNT-β-catenin signaling pathways in vivo. Kaplan-Meier survival analysis using liver cancer patient data from two clinical datasets confirmed that patients with low NR2E3 expression exhibited increased WNT-β-catenin signaling activation, associated with adverse clinical outcomes. These findings highlight NR2E3 as a crucial tumor suppressor gene in hepatocellular carcinoma (HCC), primarily restraining WNT-β-catenin signaling pathway activation to maintain epigenetic homeostasis and contribute to HCC development. Our results prove NR2E3's critical role in liver cancer pathogenesis by regulating WNT-β-catenin signaling pathways and epigenetic equilibrium maintenance. The Formaldehyde Assisted Isolation of Regulatory Elemens (FAIRE)-Seqwas performed using control (shCT) and NR2E3-depleted (shNR2E3) HepG2 cells.

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The Loss of an orphan Nuclear Receptor augments Wnt/β-Catenin signaling via epigenetic dysregulation that promotes Sp1 and Myc interactions in Hepatocellular Carcinoma Development [RNA-seq]

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The Loss of an Orphan Nuclear Receptor NR2E3 Augments Wnt/β-catenin Signaling via Epigenetic Dysregulation that Enhances Sp1-β catenin-p300 Interactions in Hepatocellular Carcinoma.

Project description:The orphan nuclear receptor NR2E3 (Nuclear receptor subfamily 2 group E, Member 3) is an epigenetic player that modulates chromatin accessibility to activate p53 during liver injury. Nonetheless, a precise tumor suppressive and epigenetic role of NR2E3 in hepatocellular carcinoma (HCC) development remains unclear. HCC patients expressing low NR2E3 exhibit unfavorable clinical outcomes, aligning with heightened activation of the Wnt/β-catenin signaling pathway. The murine HCC models utilizing NR2E3 knockout mice consistently exhibits accelerated liver tumor formation accompanied by enhanced activation of Wnt/β-catenin signaling pathway and inactivation of p53 signaling. At cellular level, the loss of NR2E3 increases the acquisition of aggressive cancer cell phenotype and tumorigenicity and upregulates key genes in the WNT/β-catenin pathway with increased chromatin accessibility. This event is mediated through increased formation of active transcription complex involving Sp1, β-catenin, and p300, a histone acetyltransferase, on the promoters of target genes. These findings demonstrate that the loss of NR2E3 activates Wnt/β-catenin signaling at cellular and organism levels and this dysregulation is associated with aggressive HCC development and poor clinical outcomes. In summary, NR2E3 is a novel tumor suppressor with a significant prognostic value, maintaining epigenetic homeostasis to suppress the Wnt/β-catenin signaling pathway that promotes HCC development.

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