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Interactomic analysis of PEAK3 pseudo-kinase

ABSTRACT: The aim of the project was to identify the interactome of PEAK3 pseudokinase that was expressed in various cancer cells.

INSTRUMENT(S): Q Exactive HF-X

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Functional Proteomics Platform FPP

LAB HEAD: Serge Roche

PROVIDER: PXD029417 | Pride | 2022-01-04

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	PEAK3_190118_H3_GFP.raw	Raw
	PEAK3_190118_H3_PEAK3.raw	Raw
	PEAK3_190321_HFX2_E1.raw	Raw
	PEAK3_190321_HFX_E2.raw	Raw
	PEAK3_190321_HFX_E3.raw	Raw

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1 - 5 of 18

Publications

SHED-Dependent Oncogenic Signaling of the PEAK3 Pseudo-Kinase.

Ounoughene Youcef Y Fourgous Elise E Boublik Yvan Y Saland Estelle E Guiraud Nathan N Recher Christian C Urbach Serge S Fort Philippe P Sarry Jean-Emmanuel JE Fesquet Didier D Roche Serge S

Cancers 20211217 24

The PEAK1 and Pragmin/PEAK2 pseudo-kinases have emerged as important components of the protein tyrosine kinase pathway implicated in cancer progression. They can signal using a scaffolding mechanism that involves a conserved split helical dimerization (SHED) module. We recently identified PEAK3 as a novel member of this family based on structural homology; however, its signaling mechanism remains unclear. In this study, we found that, although it can self-associate, PEAK3 shows higher evolutiona ...[more]

PMID: 34944965

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Project description:In an effort to identify oncogenic protein kinase drivers in triple negative breast cancer (TNBC), we undertook mass spectrometry (MS)-based proteomic profiling across a large panel of TNBC cell lines. This revealed marked variation in expression of the multidomain pseudokinase Nuclear Receptor Binding Protein 1 (NRBP1). Interrogation of publicly-available data determined that NRBP1 gene expression is higher in TNBC than in luminal breast cancers and positively associates with poor prognosis in TNBC patients. Gain and loss of function experiments characterized NRBP1 as a positive regulator of TNBC cell migration and invasion. In addition, NRBP1 knockdown reduced colony formation in vitro and moreover, markedly impaired growth of TNBC orthotopic xenografts as well as lung colonization in an experimental metastasis model. To interrogate the signalling mechanism of NRBP1, we applied BioID/MS profiling, identifying P-Rex1, a guanine nucleotide exchange factor for Rac1 and Cdc42, as a NRBP1 binding partner. Importantly, NRBP1 overexpression enhanced levels of GTP-bound Rac1 and Cdc42 in a P-Rex1-dependent manner, while NRBP1 knockdown reduced their activation. In addition, NRBP1 associated with P-Rex1, Rac1 and Cdc42, suggesting a scaffolding function for this pseudokinase. NRBP1-mediated promotion of cell migration and invasion was P-Rex1-dependent, while constitutively-active Cdc42 wholly/or partially rescued the effect of NRBP1 knockdown on cell migration/invasion and colony formation, respectively. Generation of reactive oxygen species via a NRBP1/P-Rex1 pathway was implicated in these oncogenic roles of NRBP1. Overall, these findings define a new function for NRBP1 and a novel oncogenic signalling pathway in TNBC that may be amenable to therapeutic intervention.

2023-05-05 | PXD032168 | Pride

Melanoma BRAFV600E induced proteome

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Expression microarray analysis of RHOXF1 and RHOXF2 transfected HEK293 cells

Project description:The X-linked reproductive homeobox (RHOX) gene cluster encodes transcription factors displaying preferential expression in reproductive tissues. They have important roles in human male fertility based on phenotypic defects of Rhox-mutant mice and the finding that aberrant RHOX promoter methylation is strongly associated with abnormal human sperm parameters. The aim of this study was to analyze the molecular mechanism of RHOX action in humans. Using genome-wide analysis, we investigated the identity of genes regulated by the known human RHOX transcription factors: RHOXF1 and RHOXF2/2B. HEK293 cells were transiently transfected with either RHOX expression (RHOXF1; RHOXF2) or an empty control vector. Afterwards, differently expressed genes were identified by microarray analysis after 24h and 48h of transfection. Thereby we could identify genes that are differently regulated in response to RHOX overexpression. Total RNA was isolated from RHOX (RHOXF1; RHOXF2) and control transfected HEK293 cells after 24h and 48h of transfection. Affymetrix GeneChip Human Exon 1.0 ST arrays were used to evaluate changes in mRNA expression in RHOX transfected samples compared to control transfected samples (analyzed in biological triplicates). Data were processed and analyzed using Affymetrix Gene Expression Console and Affymetrix transcriptome analysis console.

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Histone ChIP NS5 Ascl1-ERT2

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IMR90 hTERT

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Rapid, optimized interactomic screening.

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Transcriptional targets of oncogenic RAS proteins that mediate their ability to induce cellular transformation

Project description:Mutations in the NRAS oncogene are present in up to 20% of melanoma. Here, we show that interferon alpha-inducible protein 6 (IFI6) is necessary for NRASQ61K-induced transformation and melanoma growth. IFI6 was transcriptionally upregulated by NRASQ61K, and knockdown of IFI6 resulted in DNA replication stress due to dysregulated DNA replication via E2F2. This stress consequentially inhibited cellular transformation and melanoma growth via senescence or apoptosis induction depending on the RB and p53 pathway status of the cells. NRAS-mutant melanoma were significantly more resistant to the cytotoxic effects of DNA replication stress-inducing drugs, and knockdown of IFI6 increased sensitivity to these drugs. Pharmacological inhibition of IFI6 expression by the MEK inhibitor trametinib, when combined with DNA replication stress-inducing drugs, blocked NRAS-mutant melanoma growth. Collectively, we demonstrate that IFI6, via E2F2 regulates DNA replication and melanoma development and growth, and this pathway can be pharmacologically targeted to inhibit NRAS-mutant melanoma. MEL-ST cells expressing either empty vector or mutant oncogenic RAS genes (HRAS v12, KRAS v12, NRAS Q61K) were used to isolate total RNA. The RNA was then used to perform gene expression analyses using the Illumina HumanHT-12 V4.0 Expression BeadChip array.

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