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Elucidation of the BMI1 interactome identifies novel regulatory roles in glioblastoma

ABSTRACT: Elucidation of the BMI1 interactome identifies novel regulatory roles in glioblastoma

PROVIDER: PRJNA670408 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12858005_1.fastq.gz	Fastqsanger.gz
	SRR12858005_2.fastq.gz	Fastqsanger.gz
	SRR12858006_1.fastq.gz	Fastqsanger.gz
	SRR12858006_2.fastq.gz	Fastqsanger.gz
	SRR12858007_1.fastq.gz	Fastqsanger.gz

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Elucidation of the BMI1 interactome identifies novel regulatory roles in glioblastoma

Project description:Glioblastoma (GBM) is the most common and aggressive intrinsic brain tumour in adults. Epigenetic mechanisms controlling normal brain development are often dysregulated in GBM. Among these, BMI1, a structural component of the Polycomb Repressive Complex 1 (PRC1), which promotes the H2AK119ub catalytic activity of Ring1B, is upregulated in GBM and its tumorigenic role has been shown in vitro and in vivo. Here, we have used protein and chromatin immunoprecipitation followed by mass spectrometry (MS) analysis to elucidate the protein composition of PRC1 in GBM and CRISPR/dCAS9-mediated modulation of BMI1 to assess its influence on protein interactions. We show that while well-established BMI1 functions such as control of cell proliferation and cell adhesion are PRC1-dependent, novel regulatory functions in mRNA splicing and cholesterol transport are PRC1 independent and may represent novel targetable mechanisms in GBM.

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The deubiquitinase USP22 stabilizes BMI1 polycomb ring finger oncoprotein to confer cancer stem cell traits and glioblastoma progression

Project description:Glioblastoma (GBM) is the most common and aggressive primary brain tumor with limited therapeutic options, possibly because of the highly tumorigenic subpopulations of stem cell-like cells. Mechanisms that sustain cancer stem cells are crucial to tumor progression. The polycomb group protein BMI1 (BMI1 proto-oncogene, polycomb ring finger) maintains cancer hallmarks including the glioblastoma stem-like cell (GSC) state. Ubiquitin-specific protease 22 (USP22) is highly expressed in and required for the maintenance of cancer stem cells (CSCs). Previously, we observed that forced expressed microRNA-218 in glioblastoma cells led to suppressed BMI1 expression. However, the pathways engaged by USP22 or driving BMI1 accumulation in GSCs remained elusive. Here, we found USP22 to be a novel deubiquitylase of BMI1. USP22 directly deubiquitylates and stabilizes BMI1. USP22 protein levels are elevated in tumor neurosphere. USP22 depletion induces BMI1 destabilization, and results in the inhibition of GSCs self-renewal by regulating a broad range of genes involved in glioma stemness and progression. Xenograft analyses using U87MG cells showed that both USP22 and BMI1 depletion attenuated tumor growth. Clinically, the expression levels of USP22 and BMI1 were positively correlated with those common targets like POSTN, HEY2, or PDGFRA and inversely correlated with ATF3 in human glioblastoma specimens. Taken together, our data reveals that USP22 functions as a novel deubiquitylase of BMI1 and inhibits self-renewal of GSCs by stabilizing BMI1. These findings also indicate that the USP22-BMI1 axis has a critical role in glioma tumorigenesis and that targeting the axis may provide a new therapeutic approach for human glioblastoma.

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