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Hypoxia-induced phase separation of ZHX2 drives 3D chromatin remodeling and cancer metastasis (ChIP-Seq)

ABSTRACT: Hypoxia-induced phase separation of ZHX2 drives 3D chromatin remodeling and cancer metastasis (ChIP-Seq)

PROVIDER: PRJNA1083514 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28215169_1.fastq.gz	Fastqsanger.gz
	SRR28215169_2.fastq.gz	Fastqsanger.gz
	SRR28215170_1.fastq.gz	Fastqsanger.gz
	SRR28215170_2.fastq.gz	Fastqsanger.gz
	SRR28215171_1.fastq.gz	Fastqsanger.gz

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Hypoxia-induced phase separation of ZHX2 drives 3D chromatin remodeling and cancer metastasis (ChIP-Seq)

Project description:Hypoxia and dysregulation of three-dimensional (3D) chromatin architecture can both activate oncogenic transcriptomic profiles, thus contributing to tumor malignancy. But how hypoxia regulates 3D chromatin architecture remains unknown. Here, we find that the transcription factor, zinc fingers and homeoboxes 2 (ZHX2), generates liquid-liquid phase separation (LLPS) under hypoxia, thus promoting its occupancy on chromatin and activating transcription for a cluster of oncogenes, that is enriched by metastatic genes distinct from targets of hypoxia-inducible factor (HIF) and pathologically relevant to breast cancer. Mechanistically, hypoxia induces the LLPS of ZHX2 via a proline-rich intrinsically disordered region (IDR) in the nuclear localization sequence (NLS), thereby enhancing the phosphorylation of ZHX2 at S625 and S628 that incorporates CCCTCbinding factor (CTCF) in condensates to reorganize chromatin looping, consequently resulting in oncogenic super-enhancer formation and breast cancer metastasis. This fundamental mechanism provides significant insight into oncogene activation and suggests a phase separation-based therapeutic strategy for cancer.

2025-03-18 | GSE260793 | GEO

Hypoxia-induced phase separation of ZHX2 drives 3D chromatin remodeling and cancer metastasis (ATAC-Seq)

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Hypoxia-induced phase separation of ZHX2 drives 3D chromatin remodeling and cancer metastasis (Hi-C)

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Hypoxia-induced phase separation of ZHX2 drives 3D chromatin remodeling and cancer metastasis (RNA-Seq)

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Hypoxia-induced phase separation of ZHX2 drives 3D chromatin remodeling and cancer metastasis

Project description:Hypoxia-induced phase separation of ZHX2 drives 3D chromatin remodeling and cancer metastasis

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Hypoxia-induced phase separation of ZHX2 drives 3D chromatin remodeling and cancer metastasis (RNA-Seq)

Project description:Hypoxia-induced phase separation of ZHX2 drives 3D chromatin remodeling and cancer metastasis (RNA-Seq)

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Hypoxia-induced phase separation of ZHX2 drives 3D chromatin remodeling and cancer metastasis (ATAC-Seq)

Project description:Hypoxia-induced phase separation of ZHX2 drives 3D chromatin remodeling and cancer metastasis (ATAC-Seq)

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Hypoxia-induced phase separation of ZHX2 drives 3D chromatin remodeling and cancer metastasis

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

2025-03-18 | GSE260795 | GEO

USP13 Promotes Deubiquitination of ZHX2 and Tumorigenesis in Kidney Cancer

Project description:Clear cell renal cell carcinoma (ccRCC) is characterized by loss of tumor suppressor Von Hippel Lindau (VHL) function. VHL is the component of E3 ligase complex that promotes the ubiquitination and degradation of hypoxia inducible factor alpha (including HIF1alpha and HIF2alpha) and Zinc Fingers And Homeoboxes 2 (ZHX2). Our recent research showed that ZHX2 contributed to ccRCC tumorigenesis in a HIF independent manner. However, it remains unknown whether ZHX2 can be regulated through deubiquitination. Here we performed a deubiquitinase (DUB) cDNA library binding screen and identified USP13 as a novel DUB that bound ZHX2 and promoted ZHX2 deubiquitination. As a result, USP13 promoted ZHX2 protein stability in an enzymatically dependent manner and depletion of USP13 led to ZHX2 downregulation in ccRCC. Functionally, USP13 depletion led to decreased cell proliferation measured by 2-D colony formation and 3-D anchorage independent growth. USP was a critical effector on maintaining kidney tumorigenesis in an orthotopic xenograft model and its depletion led to both decreased primary kidney tumorigenesis and spontaneous lung metastasis. Our results suggest that USP13 is a potential new therapeutic target in ccRCC.

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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.

2021-05-25 | GSE175487 | GEO

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