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Genome-wide maps of acetylated lysine 27 of Histone 3 (ChIP-seq) and gene expression profiling (RNA-seq) in wildtype and USP7-KO H1299 lung cancer lines

ABSTRACT: Ubiquitin Specific Protease 7 (USP7), also named as herpesvirus-associated ubiquitin-specific protease (HAUSP), is one of the most abundant deubiquitinase and plays multifaceted roles in many cellular functions, including the protein homeostasis, DNA repair, gene transcription, and oncogenic pathways. To investigate the role of USP7 in p53-deficient lung cancer cells, the CRISPR/Cas9-mediated gene editing was employed to inactivate the USP7 locus in H1299 cells. The alterations of transcriptional enhancers and gene expression were analyzed by H3K27ac ChIP-seq and RNA-seq, respectively, in wildtype and USP7-KO H1299 lung cancer cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE172506 | GEO | 2021/09/16

REPOSITORIES: GEO

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Transcriptome profiling in USP7 inhibitor (P22077)-treated H1299 and HeLa cells

Project description:To investigate the molecular pathway signature responsive to pharmacological inhibition of USP7, we analyzed transcriptome in P22077 (a USP7 selective inhibitor)-treated H1299 and HeLa cells.

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Project description:USP7, a dominant DUB activity in 3T3-L1 adipocytes and in mouse adipose tissue, increases Tip60 protein levels, and deubiquitinates Tip60 both in intact cells and in vitro. Treatment with a pan deubiquitinase (DUB) inhibitor, or knockdown of USP7, decreases adipogenesis. Transcriptome analysis reveals a common set of cell cycle genes to be co-regulated by both Tip60 and USP7. Knock down of either factor results in impaired mitotic clonal expansion, an early step in adipogenesis. These results therefore reveal deubiquitination of a transcriptional coregulator to be a key mechanism in the regulation of early adipogenesis Mature 3T3-L1 adipocytes were subjected to RNAi-mediated knock down with control(C), USP7(U)- or Tip60(T)-specific oligonucleotides. For this, 4 replicates of differentiated 3T3-L1 cells were transfected with Amaxa technology. Two days after transfection cells were washed twice with PBS twice and lysed in 0.5ml Trizol (Invitrogen). mRNA expression of Tip60 and USP7 was assessed by qRT-PCR. Amplified cRNA samples were labeled with either cy3 or cy5 and put on microarray together with and oppositely labeled common reference sample consisting of cRNA derived from undifferentiated 3T3-L1 cells.

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USP7 counteracts the activation of the mitotic program

Project description:Chemical inhibitors of the deubiquitinase USP7 are currently being developed as anticancer agents, due to their capacity to activate P53. Regardless of this activity, USP7 inhibitors also generate DNA damage in a p53-independent manner. However, the mechanism of this genotoxicity remains unknown. Surprisingly, even if USP7 inhibitors stop DNA replication, this occurs concomitant to a premature activation of mitotic kinases such as CDK1, which impairs chromosome segregation and is toxic for mammalian cells. Mechanistically, we show that USP7 interacts with the phosphatase PP2A and regulates its function. Accordingly, USP7 or PP2A inhibition trigger similar changes on the phosphoproteome, with a particular bias towards mitotic targets. Supporting our model, the toxicity of USP7 inhibitors is alleviated by lowering CDK1 activity or by the chemical activation of PP2A. Our work sheds light into the mechanism of action of USP7 inhibitors and provides the first example of triggering premature mitotic entry through perturbation of ubiquitin signaling.

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