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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]

Project description:In order to explore the biological function and molecular mechanism of ZHX2 in VSMCs,in this study, we overexpressed ZHX2 in primery VSMCs used chromatin immunoprecipitation sequencing (ChIP-seq) methods to systematically investigate the downstream targets of ZHX2.

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Role of ZHX2 in VSMCs

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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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Role of ZHX2 in VSMCs

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

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Epigenetic Regulation of VSMCs by Arid3a: Insights from RNA-seq Analyses

Project description:This study employs RNA-seq to investigate the transcriptional effects of Arid3a in Vascular Smooth Muscle Cells (VSMCs), revealing a comprehensive signature of gene expression. We identified 394 genes that were downregulated and 227 that were upregulated in response to Arid3a knockdown, shedding light on its regulatory network. The RNA-seq data highlighted the key role of Arid3a in controlling the dynamics of actin filaments, which has implications for processes such as cell adhesion and the cAMP signaling pathway.

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Project description:Diffuse large B-cell lymphoma (DLBCL), the most common B-cell non-Hodgkin lymphoma (B-NHL), is characterized by strong aggression, high heterogeneity and poor prognosis. Consequently, there is an urgent need to identify crucial therapeutic targets. Here, we found that the transcription factor Zinc-finger and homeoboxes 2 (ZHX2) is highly expressed in DLBCL. Subsequently, ZHX2 was proven to be critical for promoting DLBCL cells proliferation by inhibiting ferroptosis. Mechanistically, ZHX2 binds to the promoter region of the solute carrier family 3-member 2 (SLC3A2) gene through liquid-liquid phase separation (LLPS) and activates its function to negatively regulate ferroptosis. Furthermore, we constructed lipid nanoparticles Zhx2-siRNA@LNP targeting DLBCL, which effectively inhibited the growth of the tumor in vivo. In summary, our study indicated that LLPS of ZHX2 protects DLBCL against ferroptosis through induction of SLC3A2, and disturbing it with Zhx2-siRNA@LNP could significantly repress DLBCL, providing a promising therapeutic strategy for DLBCL.

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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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