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MY-COMP, an inhibitor of the transcriptional activity of YAP-B-MYB, identifies NEK2 as a novel mediator of YAP oncogenesis in uveal melanoma cells [RNA-seq]

ABSTRACT: MY-COMP, an inhibitor of the transcriptional activity of YAP-B-MYB, identifies NEK2 as a novel mediator of YAP oncogenesis in uveal melanoma cells [RNA-seq]

PROVIDER: PRJNA947601 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23940450.fastq.gz	Fastqsanger.gz
	SRR23940451.fastq.gz	Fastqsanger.gz
	SRR23940452.fastq.gz	Fastqsanger.gz
	SRR23940453.fastq.gz	Fastqsanger.gz
	SRR23940454.fastq.gz	Fastqsanger.gz

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MY-COMP, an inhibitor of the transcriptional activity of YAP-B-MYB, identifies NEK2 as a novel mediator of YAP oncogenesis in uveal melanoma cells [RNA-seq]

Project description:Activation of YAP is frequently observed in cancer and is associated with poor outcomes, making it an attractive target for therapeutic intervention. Previous studies have mainly focused on blocking the interaction of YAP with TEAD transcription factors. Here we took a different approach by interfering with the binding of YAP to the transcription factor B-MYB using MY-COMP, a fragment of B-MYB containing the YAP binding domain fused to a nuclear localization signal. We found that expression of MY-COMP inhibited the binding of B-MYB to YAP, resulting in growth defects, nuclear abnormalities and polyploidization in HeLa cells. Additionally, MY-COMP interfered with normal cell cycle progression of YAP-dependent uveal melanoma cells, but its effects were much weaker in YAP-independent cutaneous melanoma cell lines. MY-COMP antagonized the YAP-dependent expression of MMB-regulated cell cycle genes, providing an explanation for the observed phenotypes. We identified NIMA-related kinase (NEK2) as a candidate target downstream of YAP and B-MYB, contributing to the transformation of YAP-dependent uveal tumor cell lines. Overall, our findings suggest that targeting selected YAP-MMB regulated genes such as NEK2 or inhibiting the WW-domains of YAP to suppress YAP-regulated cell cycle genes could provide a novel mechanism to antagonize the pro-tumorigenic functions of YAP.

2024-03-06 | GSE227973 | GEO

MY-COMP, an inhibitor of the transcriptional activity of YAP-B-MYB, identifies NEK2 as a novel mediator of YAP oncogenesis in uveal melanoma cells [CUT&RUN]

2024-03-06 | GSE227972 | GEO

MY-COMP, an inhibitor of the transcriptional activity of YAP-B-MYB, identifies NEK2 as a novel mediator of YAP oncogenesis in uveal melanoma cells

Project description:MY-COMP, an inhibitor of the transcriptional activity of YAP-B-MYB, identifies NEK2 as a novel mediator of YAP oncogenesis in uveal melanoma cells

| PRJNA947598 | ENA

MY-COMP, an inhibitor of the transcriptional activity of YAP-B-MYB, identifies NEK2 as a novel mediator of YAP oncogenesis in uveal melanoma cells [CUT&RUN]

Project description:MY-COMP, an inhibitor of the transcriptional activity of YAP-B-MYB, identifies NEK2 as a novel mediator of YAP oncogenesis in uveal melanoma cells [CUT&RUN]

| PRJNA947600 | ENA

Targeting NEK2 impairs oncogenesis and radioresistance via inhibiting the Wnt1/β-catenin signaling pathway in cervical cancer

Project description:We report that NEK2 protein level is overexpressed and correlated with the tumor stage and lymph node metastasis in cervical cancer. Furthermore, we provided evidence that NEK2-depleted cervical cancer cells exhibit impaired oncogenesis and enhanced radiosensitivity. Using RNA sequencing, we identify Wnt1 as a key downstream effector of NEK2. Knockdown of NEK2 downregulates the mRNA and protein levels of Wnt1, thereby inhibiting the activation of the Wnt/β-catenin signaling pathway. More importantly, the observed consequences induced by NEK2 depletion in cervical cancer cells can be partially rescued by Wnt1 overexpression. Taken together, these results demonstrate that NEK2 activates the Wnt/β-catenin signaling pathway via Wnt1 to drive oncogenesis and radioresistance in cervical cancer, indicating that NEK2 may be a promising target for the radiosensitization of cervical cancer.

2021-04-30 | GSE148531 | GEO

MY-COMP, an inhibitor of the transcriptional activity of YAP-B-MYB, identifies NEK2 as a novel mediator of YAP oncogenesis in uveal melanoma cells

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

2024-03-06 | GSE227974 | GEO

MY-CLIP verification study

Project description:Comparison between BrdU-CLIP and MY-CLIP for HNRNPU, and MY-CLIP performance for HNRNPC

2020-03-31 | GSE138649 | GEO

A comprehensive enhancer screen identifies TRAM2 as a key mediator of YAP oncogenesis

Project description:Frequent activation of the co-transcriptional factor YAP is observed in a large number of solid tumors. Activated-YAP associates with enhancer loci via TEAD4-DNA-binding protein, and stimulates cancer aggressiveness. Although thousands of YAP/TEAD4 binding-sites were annotated, their functional importance is unknow. Here, we implemented a genetic approach to uncover functions of YAP/TEAD4-associated enhancers, demonstrated its robustness, and used it to reveal a network of enhancers required for YAP-mediated proliferation. We focused on Enhancer TRAM2, as its target gene TRAM2 showed the strongest expression-correlation with YAP in nearly all tumor types. Interestingly, TRAM2 phenocopied YAP-induced cell proliferation, migration and invasion phenotypes, and correlated with poor patient survival. Mechanistically, we identified FSTL-1 as a major direct client of TRAM2 that is involved in these phenotypes. Thus, TRAM2 is a key novel mediator of YAP-induced oncogenic proliferation and cellular invasiveness.

2021-01-14 | PXD018559 | Pride

NEK2 regulates triple negative breast cancer transcriptome.

Project description:NEK2 is a mitotic kinase that is upregulated and mislocalized in the nucleus of human cancer cells. NEK2 modulates expression and activity of both transcription and splicing factors in cancer cells, nevertheless whether this kinase affects transcriptome regulation genome widely and whether this activity concurs to its oncogenic activity is still unknown. Herein, by high-throughput RNA sequencing analysis of MDA-MB-231 cells transiently silenced for NEK2 we uncover an extensive modulation of triple-negative breast cancer cell transcriptome by this kinase.

2021-12-21 | GSE140803 | GEO

Phosphoproteomics analysis of TAMs with NEK2 overexpression

Project description:NEK2 is considered a key factor in the maintenance of development and function of B cells in multiple myeloma (MM). Importantly, we previously demonstrated that PD-L1 is a substrate of NEK2, and combinatorial inhibition of NEK2 and PD-L1 largely improves the therapeutic efficacy of pancreatic cancer in pre-clinical models. But the expression and function of NEK2 in HCC-related TAMs have not yet been studied. This analysis revealed changes in the proteome due to the overexpression of NEK2 in TAMs, providing a valuable reference for further functional investigations.

2025-05-26 | PXD054708 | Pride

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