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Chemokine receptor CXCR7 activates Aurora Kinase A and promotes neuroendocrine prostate cancer growth

ABSTRACT: Chemokine receptor CXCR7 activates Aurora Kinase A and promotes neuroendocrine prostate cancer growth

PROVIDER: PRJNA819102 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18456870.fastq.gz	Fastqsanger.gz
	SRR18456871.fastq.gz	Fastqsanger.gz
	SRR18456872.fastq.gz	Fastqsanger.gz
	SRR18456873.fastq.gz	Fastqsanger.gz
	SRR18456874.fastq.gz	Fastqsanger.gz

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Chemokine receptor CXCR7 activates Aurora Kinase A and promotes neuroendocrine prostate cancer growth

Project description:CXCR7, an atypical chemokine receptor (ACKR3), is up-regulated in NEPC, and its expression is associated with molecular markers of NEPC and cell proliferation. Transcriptomic analyses revealed a major role of CXCR7 in regulating downstream genes involved in the cell cycle and mitotic spindle. Membrane-bound CXCR7 is known to recruit β-arrestin (ARRB2), and the complex internalizes into clathrin-coated vesicles where they act as a scaffold for cytoplasmic kinase assembly and substrate activation. We identify Aurora Kinase A (AURKA) as a top candidate that is binding to and activated by CXCR7-ARRB2. Immunofluorescence confocal microscopy detected high-density CXCR7, ARRB2, and AURKA in the pericentrosomal area with focal staining of ARRB2 and ARUKA at centrosomes. Mass spectrometry showed that CXCR7 interacts with many proteins associated with intracellular vesicles, microtubules, and Golgi apparatus. CXCR7-ARRB2-containing vesicles traffic along the microtubules to the perinuclear Golgi apparatus, where CXCR7-ARRB2 interacts with AURKA to promote its activation and cell growth. Finally, we showed that pharmacological inhibitors of AURKA abolish CXCR7-driven tumor growth. Our study reveals CXCR7-mediated activation of AURKA and establishes CXCR7 and its downstream kinases as critical targets for therapeutic intervention in CRPC or NEPC patients.

2023-05-14 | GSE199274 | GEO

Chemokine receptor CXCR7 activates Aurora Kinase A and promotes neuroendocrine prostate cancer growth.

Project description:CXCR7 is an atypical chemokine receptor that recruits β-arrestin (ARRB2) and internalizes into clathrin-coated intracellular vesicles where the complex acts as a scaffold for cytoplasmic kinase assembly and signal transduction. Here, we report that CXCR7 was elevated in the majority of prostate cancer (PCa) cases with neuroendocrine features (NEPC). CXCR7 markedly induced mitotic spindle and cell cycle gene expression. Mechanistically, we identified Aurora Kinase A (AURKA), a key regulator of mitosis, as a novel target that was bound and activated by the CXCR7-ARRB2 complex. CXCR7 interacted with proteins associated with microtubules and golgi, and, as such, the CXCR7-ARRB2-containing vesicles trafficked along the microtubules to the pericentrosomal golgi apparatus, where the complex interacted with AURKA. Accordingly, CXCR7 promoted PCa cell proliferation and tumor growth, which was mitigated by AURKA inhibition. In summary, our study reveals a critical role of CXCR7-ARRB2 in interacting and activating AURKA, which can be targeted by AURKA inhibitors to benefit a subset of patients with NEPC.

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Phase II Trial of the Aurora Kinase A Inhibitor Alisertib for Castration Resistant and Neuroendocrine Prostate Cancer

Project description:<p>Neuroendocrine prostate cancer (NEPC) is an aggressive variant of prostate cancer that may develop de novo or as a mechanism of treatment resistance. N-myc is capable of driving NEPC progression. Alisertib inhibits the interaction between N-myc and its stabilizing factor Aurora-A, inhibiting N-myc signaling, and suppressing tumor growth. In this single arm, multi-institutional open label phase 2 clinical trial of alisertib, sixty men were treated with alisertib 50mg twice daily for 7 days every 21-days. Eligibility included metastatic prostate cancer and at least one: small cell neuroendocrine morphology; ≥50% neuroendocrine marker expression; new liver metastases without PSA progression; elevated serum neuroendocrine markers. The primary endpoint was six-month radiographic progression free survival. Pre-treatment biopsies were evaluated by whole exome and RNA-seq.</p>

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Expression profiling, U2OS, Aurora kinase and p38 inhibitor response

Project description:U-2 OS (human osteosarcoma cell line) were treated with ZM447439 (an aurora kinase inhibitor), SB202190 (a p38 inhibitor) or ZM447439+SB202190 and resulting changes in gene expression were profiled.

2017-07-01 | E-MTAB-1210 | biostudies-arrayexpress

CHD1 Alters Sensitivity to Aurora Kinase A Inhibitors

Project description:In this study, we sought to understand the impact of CHD1 on sensitivity to Aurora A inhibitors in prostate and other cancers and underlying mechanisms

2023-10-16 | GSE186633 | GEO

Heteractis aurora

Project description:Heteractis aurora

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Transriptome profiling of mutant p53 skin deficient in AURORA-A KINASE

Project description:We performed next-generation sequencing of RNA to determine the transcriptional changes in hyperplastic mutant p53 skin after the epithelial deletion of the AURORA-A Kinase gene in mice.

2018-10-30 | GSE106281 | GEO

Heteractis aurora

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CGH Analysis of Murine Squamous Cell Carcinoma: Control vs. Tumors overexpressing Aurora Kinase A

Project description:Genomic alterationsin murine skin Squamous Cell Carcinoma(SCC) generated were analyzed from mice that expressed human Aurora Kinase A under control of Keratin 14 driven and RU486 inducible GLP65 activator protein. Monogenic GLP65 (control) and bigenic GLP65; Aurora-A mice were treated with DMBA once and thrice per week with TPA and RU486 to generate SCCs.

2010-05-27 | GSE16342 | GEO

Aurora kinase A is upregulated in cutaneous T-cell lymphoma and represents a potential therapeutic target

Project description:Cutaneous T-cell lymphomas form a heterogeneous group of non-Hodgkin lymphomas characterized by only poor prognosis in advanced stage. Despite significant progress made in the identification of novel genes and pathways involved in the pathogenesis of cutaneous lymphoma, the therapeutic value of these findings has still to be proven. Here, we demonstrate by gene expression arrays that aurora kinase A is one of highly overexpressed genes of the serine/threonine kinase in CTCL. The finding was confirmed by qualitative RT-PCR, Western blotting and immunohistochemistry in CTCL cell lines and primary patient samples. Moreover, treatment with a specific aurora kinase A inhibitor blocks cell proliferation by inducing cell cycle arrest in G2 phase as well as apoptosis in CTCL cell lines. These new data provide a promising rationale for using aurora kinase A inhibition as a therapeutic modality of CTCL. 14 lesional skin biopsies of different MF patients (patch=3, plaque=6, tumor=4) and 9 healthy controls. Comparison between Cutaneus Tcell Lymphoma Samples and Healthy Control Tissue

2015-03-31 | E-GEOD-59307 | biostudies-arrayexpress

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