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Targeting fatty acid synthase suppresses tumor development in NF2/CDKN2A-deficient malignant pleural mesothelioma

ABSTRACT: To investigate the effect of cerulenin in NF2/p16 on gene expression, we have emoloyed whole genomic microarray expression profiling using HOMC-B1 and MeT-5Acells

ORGANISM(S): Homo sapiens

PROVIDER: GSE307912 | GEO | 2025/09/19

REPOSITORIES: GEO

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Establishment and characterization of NF2/CDKN2A-double knockout gene in human mesothelial cell line generated by using CRISPR/Cas9 technology

Project description:To investigate the effect of NF2/p16 on gene expression, we have emoloyed whole genomic microarray expression profiling using MeT-5Acells

2019-12-01 | GSE135784 | GEO

Targeting fatty acid synthase suppresses tumor development in NF2/CDKN2A-deficient malignant pleural mesothelioma

Project description:Targeting fatty acid synthase suppresses tumor development in NF2/CDKN2A-deficient malignant pleural mesothelioma

| PRJNA1327792 | ENA

Inactivation of Bap1 Cooperates with Losses of Nf2 and Cdkn2a to Drive the Development of Pleural Malignant Mesothelioma in Conditional Mouse Models

Project description:Mutations/deletions of BAP1, CDKN2A, and NF2 are the most frequent genetic lesions in human MM. We introduced various combinations of these deletions in the pleura of conditional knockout (CKO) mice, focusing on the contribution of Bap1 loss.

2019-05-30 | GSE131942 | GEO

De Novo Pyrimidine Synthesis Is a Collateral Metabolic Vulnerability in NF2-deficient Mesothelioma

Project description:Pleural mesothelioma (PM) is one of the deadliest cancers, with limited therapeutic options due to its therapeutically intractable genome, which is characterized by the functional inactivation of tumor suppressor genes (TSGs) and high tumor heterogeneity, including diverse metabolic adaptations. However, the molecular mechanisms underlying these metabolic alterations remain poorly understood, particularly how TSG inactivation rewires tumor metabolism to drive tumorigenesis and create metabolic dependencies. Through integrated multi-omics analysis, we identify for the first time that NF2 loss of function defines a distinct PM subtype characterized by enhanced de novo pyrimidine synthesis, which NF2-deficient PM cells are critically dependent on for sustained proliferation in vitro and in vivo. Mechanistically, NF2 loss activates YAP, a downstream proto-oncogenic transcriptional coactivator in the Hippo signalling pathway, which in turn upregulates CAD and DHODH, key enzymes in the de novo pyrimidine biosynthesis pathway. Our findings provide novel insights into metabolic reprogramming in PM, revealing de novo pyrimidine synthesis as a synthetic lethal vulnerability in NF2-deficient tumors. This work highlights a potential therapeutic strategy for targeting NF2-deficient mesothelioma through metabolic intervention.

2025-07-08 | PXD063342 | Pride

De Novo Pyrimidine Synthesis Is a Collateral Metabolic Vulnerability in NF2-deficient Mesothelioma

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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.

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CDKN2A deletion remodels immune infiltrate in Diffuse Pleural Mesothelioma

Project description:RNA extracted from diagnostic tumor samples of 82 patients affected by Diffuse Pleural Mesothelioma was analyzed on the nCounter system using the PanCancer Immune Profiling Panel.

2025-09-03 | GSE302048 | GEO

Chromosomal aberration of malignant pleural mesothelioma cell lines

Project description:To identify regions that display DNA copy number alterations in malignant pleural mesothelioma (MPM), we carried out array comparative genomic hybridization (CGH) analysis with 14 MPM cell lines. Regions of genomic aberrations observed in >20% of individuals were 9p21.3, 13q12.11, 16p13, and 22q12.2 of losses. The most frequent alteration was 9p21.3, which include the p16INK4/p14ARF. The loss of 22q12.2 regions include the NF2 was observed in 3 out of 14 cell lines. In 3 cell lines, loss of 13q12.11 region which contains Large Tumor Suppressor, homolog 2 (LATS2) was detected.

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Chromosomal aberration of malignant pleural mesothelioma cell lines

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Effect of Fak1/Ptk2 knockout in a mouse model of NF2-related schwannomatosis

Project description:NF2-related schwannomatosis (NF2-SWN) is a cancer predisposition syndrome characterized by the development of bilateral vestibular (VS) and spinal schwannomas. While benign, these tumors can cause significant morbidity and effective pharmacological treatments remain limited. Here we demonstrate that genetic ablation of focal adhesion kinase 1 (FAK1/PTK2) impairs tumor formation and preserves hearing in a murine model of NF2. Mechanistically, we show that Fak1 deletion decreases macrophage infiltration, attenuates NLRP3 inflammasome activation and suppresses the HGF-MET axis. Pharmacological inhibition of FAK with single agent VS-4718 did not significantly reduce macroscopic tumor volume, however, its use in combination with the MEK inhibitor selumetinib resulted in both a significant reduction tumor volume and the preservation of dorsal root ganglion (DRG) architecture. Our findings establish a critical role for FAK in schwannoma development and provide rationale for evaluation of combination FAK plus MEK inhibition in future clinical trials for NF2-associated schwannomas.

2025-09-17 | GSE292315 | GEO

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