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Establishment and characterization of CRISPR/Cas9-mediated Merlin/NF2 knockout human mesothelial cell line Met-5A

ABSTRACT: Establishment and characterization of CRISPR/Cas9-mediated Merlin/NF2 knockout human mesothelial cell line Met-5A

PROVIDER: PRJNA476769 | ENA |

REPOSITORIES: ENA

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Establishment and characterization of CRISPR/Cas9-mediated Merlin/NF2 knockout human mesothelial cell line Met-5A

Project description:To investigate the effect of NF2 on gene expression, we have employed whole genome microarray expression profiling using MeT-5A cells.

2018-06-20 | GSE116000 | GEO

Proteomic analysis of the NF2/Merlin Interactome by Proximity Biotinylation

Project description:Neurofibromatosis type 2 is an inherited neoplastic disease consisting of schwannomas, meningiomas, and ependymomas that is caused by inactivation of the tumor suppressor gene NF2. The NF2 gene product, merlin, has no intrinsic catalytic activity; its tumor suppressor function is mediated through the proteins with which it interacts. However, there is no consensus about which merlin interactions are necessary for tumor suppression. We used proximity biotinylation followed by mass spectrometry and direct binding assays to characterize the proteins that associate with merlin and merlin mutants in immortalized Schwann cells. We identified 52 proteins that associate with merlin, including a previously unreported merlin binding protein, ASPP2. Our results identify merlin as a component of mechanosensing signal transduction pathways in cell junctions, in the context of a specific set of structures and molecules through which it acts, in a cell type relevant to schwannoma formation.

2019-04-25 | PXD012017 | Pride

Merlin/NF2 Suppresses Tumorigenesis by Inhibiting the E3 Ubiquitin Ligase CRL4DCAF1 in the Nucleus

Project description:Current models imply that the FERM domain protein Merlin, encoded by the tumor suppressor NF2, inhibits mitogenic signaling at or near the plasma membrane. Here, we show that the closed, growth inhibitory form of Merlin accumulates in the nucleus, binds to the E3 ubiquitin ligase CRL4DCAF1, and suppresses its activity. Depletion of DCAF1 blocks the promitogenic effect of inactivation of Merlin. Conversely, enforced expression of a Merlin-insensitive mutant of DCAF1 counteracts the antimitogenic effect of Merlin. Re-expression of Merlin and silencing of DCAF1 induce a similar, tumor-suppressive program of gene expression. Tumor-derived mutations invariably disrupt Merlinâs ability to interact with or inhibit CRL4DCAF1. Finally, depletion of DCAF1 inhibits the hyperproliferation of Schwannoma cells from NF2 patients and suppresses the oncogenic potential of Merlin-deficient tumor cell lines. We propose that Merlin suppresses tumorigenesis by translocating to the nucleus to inhibit CRL4DCAF1. To examine if Merlin controls gene expression through inhibition of CRL4DCAF1, and define the general function of this ligase, we compared the gene expression program activated by expression of Merlin or by depletion of DCAF1 in Merlin-null FC-1801 mouse Schwannoma cells

2010-03-09 | E-GEOD-19305 | biostudies-arrayexpress

Transcriptome changes of endothelial cells in mouse tumor by Nf2/Merlin

Project description:To investigate the trancriptomic changes of endothelial cells (ECs) by Nf2/Merlin, Lewis Lung Carcinoma (LLC) tumor ECs from Ctrl and NF2 KO mice were sorted by FACS and single-cell RNA seq was performed.

2021-10-21 | GSE186162 | GEO

Merlin/NF2 Suppresses Tumorigenesis by Inhibiting the E3 Ubiquitin Ligase CRL4DCAF1 in the Nucleus

Project description:Current models imply that the FERM domain protein Merlin, encoded by the tumor suppressor NF2, inhibits mitogenic signaling at or near the plasma membrane. Here, we show that the closed, growth inhibitory form of Merlin accumulates in the nucleus, binds to the E3 ubiquitin ligase CRL4DCAF1, and suppresses its activity. Depletion of DCAF1 blocks the promitogenic effect of inactivation of Merlin. Conversely, enforced expression of a Merlin-insensitive mutant of DCAF1 counteracts the antimitogenic effect of Merlin. Re-expression of Merlin and silencing of DCAF1 induce a similar, tumor-suppressive program of gene expression. Tumor-derived mutations invariably disrupt Merlin’s ability to interact with or inhibit CRL4DCAF1. Finally, depletion of DCAF1 inhibits the hyperproliferation of Schwannoma cells from NF2 patients and suppresses the oncogenic potential of Merlin-deficient tumor cell lines. We propose that Merlin suppresses tumorigenesis by translocating to the nucleus to inhibit CRL4DCAF1.

2010-02-25 | GSE19305 | GEO

Gene expression signature regulated by cell density and Merlin/NF2 knockdown in HMLE cells

Project description:Merlin has been implicated in contact-dependent inhibition of proliferation To define genes regulated by Merlin and study their relationship to cell density-dependent gene expression, microarray experiments were performed after Merlin depletion in HMLE cells at both high and low cell densities. HMLE are non-transformed immortalized human mammary epithelial cells (Elenbaas et al., Genes Dev 15, 2001) HMLE cells were transfected with NF2 or scramble (control) siRNAs. 2 days later medium was changed (dense) or cells seeded in sparse conditions and RNA isolated the day after (3 days after siRNA transfection)

2015-04-01 | E-GEOD-53493 | biostudies-arrayexpress

lncRNA expression alterations in mesothelial cells treated with exosomes

Project description:To investigate whether exosomes from ovarian cancer cell lines could change lncRNA expression in mesothelial cells, exosomes from ovarian cancer cells (SKOV3 cells, A2780 cells) were added to MeT-5A cells, PBS treatment was set as blank control. Total RNAs of MeT-5A cells treated with exosomes were extracted, and then lncRNA sequencing was performed.

2021-09-01 | GSE151233 | GEO

Merlin/NF2-loss Driven Tumorigenesis Linked to CRL4(DCAF1)-Mediated Inhibition of the Hippo Pathway Components Lats1 and 2

Project description:Studies in drosophila have suggested that Merlin/NF2 suppresses tumorigenesis by activating upstream components of the Hippo pathway at or near the plasma membrane. In contrast, studies of Merlin-deficient tumor cells have indicated that Merlin suppresses tumorigenesis by entering into the nucleus where it inhibits the E3 ubiquitin ligase CRL4DCAF1. We found that CRL4DCAF1 promotes YAP and TEAD-dependent transcription by ubiquitylating and thereby inhibiting Lats1 and 2 in the nucleus. Genetic epistasis experiments and analysis of tumor-derived missense mutations indicate that this signaling connection sustains the oncogenicity of Merlin-deficient tumor cells. Analysis of clinical samples confirms that this pathway operates in NF2 mutant mesotheliomas, schwannomas and meningiomas. We conclude that de-repressed CRL4DCAF1 controls the output of the Hippo pathway by inhibiting Lats1 and 2 in the nucleus.

2014-07-15 | GSE56157 | GEO

Merlin rescue drives Wnt signalling

Project description:To investigate the effect of Merlin rescue on cell proliferation in 3D, we grew subcutaneous xenografts from NF2-deficient CH-157MN meningioma cells harboring doxycycline inducible WT-Merlin. Mice were treated with or without doxycycline and Merlin induction was confirmed 24 hours after induction with Western blot. We performed single-cell RNA sequencing on five Merlin-deficient tumors and seven Merlin rescue tumors

2023-08-07 | GSE224347 | GEO

Analysis of the transcriptomic profile of WT mouse embryonic fibroblast (MEF WT) and Nf2-knockout mouse embryonic fibroblast (MEF Nf2 KO) cell lines

Project description:Merlin is the tumor suppressor protein encoded by the NF2 gene. The expression of Merlin is remarkably decreased in metastatic breast cancer tissues irrespective of the breast cancer subtype. In order to ascribe clinical relevance, we re-capitulated the loss of Merlin in breast cancer cells. Merlin deficiency elicited a markedly invasive phenotype. In order to overcome the challenge of embryonic lethality of a total Nf2-knockout, we generated a unique mammary-specific Nf2-knockout mouse mammary tumor model. Both, the Nf2-knockout mouse embryonic fibroblasts (MEF) and Merlin-deficient breast tumor cells displayed a robust invasive phenotype. Transcriptomic assessment of Nf2-knockout MEFs revealed notable alterations in glutathione transferase and antioxidant networks indicating a role for Merlin in redox biology. This programmatic alteration resonated with the pathways that emerged from breast tumor cells engineered for Merlin deficiency.

2021-04-14 | GSE157677 | GEO

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