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Role of ZHX2 in VSMCs [RNA-seq]

ABSTRACT: Role of ZHX2 in VSMCs [RNA-seq]

PROVIDER: PRJNA1023580 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26270585_1.fastq.gz	Fastqsanger.gz
	SRR26270585_2.fastq.gz	Fastqsanger.gz
	SRR26270586_1.fastq.gz	Fastqsanger.gz
	SRR26270586_2.fastq.gz	Fastqsanger.gz
	SRR26270587_1.fastq.gz	Fastqsanger.gz

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Role of ZHX2 in VSMCs [RNA-seq]

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Role of ZHX2 in VSMCs [Chip-seq]

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Role of ZHX2 in VSMCs

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Role of ZHX2 in VSMCs

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

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Proteomic characterization of hepatic expression signatures affected in ZHX2 liver conditional knockout mice

Project description:The liver has an exceptional capacity for regeneration which is crucial for maintaining liver function. Since transcriptional regulation of genes controlling metabolism and cell division is a hallmark of liver regeneration (LR), we investigated the role of Zinc-finger and homeboxes 2 (ZHX2), a transcription factor critical for regulating liver postnatal gene expression and hepatic lipid hemostasis, in LR. Our results show that hepatocyte-specific Zhx2 knockout (Zhx2-KOhep) enhances LR after 2/3 partial hepatectomy in mice. Proteomics assays revealed higher mitochondrial oxidative phosphorylation (OXPHOS) in Zhx2-KOhep mouse livers. Oxygen consumption rate (OCR) and ATP generation assays confirmed the enhanced OXPHOS in Zhx2-KOhep mouse livers and human hepatocytes with ZHX2 knockdown.

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ZHX2 Promotes HIF1a Oncogenic Signaling in Triple-Negative Breast Cancer

Project description:Triple-negative breast cancer (TNBC) is an aggressive and highly lethal disease. Due to its heterogeneity and lack of hormone receptors or HER2 expression, it is critical to identify novel therapeutic targets in TNBC. Analysis of copy number and gene expression in tumors from The Cancer Genome Atlas suggested that ZHX2 was amplified and overexpressed in breast cancer patients. Correspondingly, we found that ZHX2 was highly expressed in TNBC cell lines and TNBC patient tissues. Functionally, depletion of ZHX2 inhibited TNBC cell growth and invasion in vitro, orthotopic tumor growth and spontaneous lung metastasis in vivo. Mechanistically, ZHX2 bound with Hypoxia inducible factor (HIF) family members and positively regulated HIF1 activity in TNBC by using loss-of-function or gain-of-function studies. Our integrated ChIP-Seq and gene expression profiling demonstrated that ZHX2 co-occupied with HIF1 on transcriptionally active promoters marked by H3K4me3 and H3K27Ac, therefore promoting gene expression. Furthermore, structural simulation and functional studies revealed that multiple residues (R491, R581 and R674) are important in regulating the phenotype of ZHX2 on TNBC tumorigenic potential, which correspond with their roles on controlling HIF1 activity in TNBC cells. These studies establish that ZHX2 activates oncogenic HIF1 signaling, therefore serving as a potential therapeutic target for TNBC.

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