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A fetal oncogene NUAK2 is an emerging target in glioblastoma

ABSTRACT: A fetal oncogene NUAK2 is an emerging target in glioblastoma

PROVIDER: PRJNA1204125 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31848739_1.fastq.gz	Fastqsanger.gz
	SRR31848739_2.fastq.gz	Fastqsanger.gz
	SRR31848740_1.fastq.gz	Fastqsanger.gz
	SRR31848740_2.fastq.gz	Fastqsanger.gz
	SRR31848741_1.fastq.gz	Fastqsanger.gz

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A fetal oncogene NUAK2 is an emerging target in glioblastoma

Project description:Glioblastoma Multiforme (GBM) is the most prevalent and highly malignant form of adult brain cancer characterized by poor overall survival rates. Effective therapeutic modalities remain limited, necessitating the need for novel treatments. Neurodevelopmental pathways have been implicated in glioma formation, with key neurodevelopmental regulators being re-expressed or co-opted during glioma tumorigenesis. Here we identified a serine/threonine kinase, NUAK family kinase 2 (NUAK2), as a fetal oncogene in mouse and human brains. We found robust expression of NUAK2 in the embryonic brain that decreases throughout postnatal stages and then is re-expressed in malignant gliomas. However, the role of NUAK2 in GBM tumorigenesis remains unclear. Here, we demonstrate that CRIPSR-Cas9 mediated NUAK2 deletion in GBM cells results in suppression of proliferation and migration, while overexpression leads to enhanced proliferation and migration in both in vitro and in vivo models. Further investigation of the downstream biological processes dysregulated in the absence of NUAK2 reveals that NUAK2 modulates extracellular matrix (ECM) components to facilitate migratory behavior. Lastly, we determined that pharmaceutical inhibition of NUAK2 is sufficient to impede the proliferation and migration of malignant glioma cells. Our results suggest that NUAK2 is an actionable therapeutic target for GBM treatment.

2025-02-12 | GSE285513 | GEO

A fetal oncogene NUAK2 is an emerging therapeutic target in glioblastoma.

Project description: Not available

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A fetal oncogene NUAK2 is an emerging therapeutic target in glioblastoma.

Project description: Not available

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A fetal oncogene NUAK2 is an emerging therapeutic target in glioblastoma

Project description: Not available

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A fetal oncogene NUAK2 is an emerging therapeutic target in glioblastoma

Project description: Not available

| S-SCDT-10_1038-S44321-025-00287-3 | biostudies-other

The proto-oncogene tyrosine kinase c-SRC facilitates glioblastoma progression by remodeling fatty acid synthesis

Project description:Increased fatty acid synthesis benefits glioblastoma malignancy. However, the coordinated regulation of cytosolic acetyl-CoA production, the exclusive substrate for fatty acid synthesis, remains unclear. Here, we show that proto-oncogene tyrosine kinase c-SRC is activated in glioblastoma and remodels cytosolic acetyl-CoA production for fatty acid synthesis. Firstly, acetate is an important substrate for fatty acid synthesis in glioblastoma. c-SRC phosphorylates acetyl-CoA synthetase ACSS2 at Tyr530 and Tyr562 to stimulate the conversion of acetate to acetyl-CoA in cytosol. Secondly, c-SRC inhibits citrate-derived acetyl-CoA synthesis by phosphorylating ATP-citrate lyase ACLY at Tyr682. ACLY phosphorylation shunts citrate to IDH1-catalyzed NADPH production to provide reducing equivalent for fatty acid synthesis. The c-SRC-unresponsive double-mutation of ACSS2 and ACLY significantly reduces fatty acid synthesis and hampers glioblastoma progression. In conclusion, this remodeling fulfills the dual needs of glioblastoma cells for both acetyl-CoA and NADPH in fatty acid synthesis and provides evidence for glioma treatment by c-SRC inhibition.

2024-07-29 | PXD054314 | Pride

The MET oncogene is a functional marker of a glioblastoma stem cell subtype and drives the invasive phenotype

Project description:Eighteen independent neurospheres derived from patients affected by primary glioblastoma were grouped into “classical”, “mesenchymal” or “proneural” subtypes according to analysis of genetic lesions and gene expression profiling. Here we show that expression of the MET oncogene, encoding the tyrosine kinase receptor for HGF, associates with mesenchymal and proneural neurospheres (Met-pos-NS). Met expression is almost absent from classical neurospheres (Met-neg-NS), and mutually exclusive with amplification and expression of the EGF receptor gene. Met-pos-NS and Met-neg-NS display distinct growth factor requirements, differentiate along divergent pathways, and generate tumors with distinctive histological features. Met-pos-NS contain a variable percentage of Met positive (Methigh) and Met negative (Metneg) cells. After purification, only Methigh cells display clonogenic ability in vitro, and regenerate neurospheres containing both Methigh and Metneg cells. After in vivo transplantation, Methigh cells display highly enriched tumorigenic potential as compared with Metneg cells. At functional level, in Methigh cells, HGF concomitantly sustains proliferation, clonogenicity, expression of self-renewal markers, migration and invasion. These data show that Met is a functional marker of glioblastoma stem cells, and a candidate target for molecular diagnosis and therapy of a glioblastoma subset. 37 samples (17 replicate samples and 1 triplicate sample)

2012-10-05 | E-GEOD-36426 | biostudies-arrayexpress

The RNA m6A reader YTHDF2 maintains oncogene expression and is a targetable dependency in glioblastoma stem cells [RNA-seq]

Project description:Glioblastoma is a universally lethal cancer driven by glioblastoma stem cells (GSCs). Here, we interrogated N6-methyladenosine (m6A) mRNA modifications in GSCs by methyl RNA-immunoprecipitation followed by sequencing (meRIP-seq) and transcriptome analysis, finding transcripts marked by m6A often upregulated. Interrogating m6A regulators, GSCs displayed preferential expression as well as in vitro and in vivo dependency of the m6A reader, YTHDF2, in contrast to normal neural stem cells (NSCs). While YTHDF2 has been reported to destabilize mRNAs, YTHDF2 stabilized the oncogene transcripts, MYC and VEGFA, in GSCs in an m6A-dependent manner. We identified IGFBP3 as a downstream effector of the YTHDF2-MYC axis in GSCs and IGF1/IGF1R inhibitor, Linsitinib, as preferentially targeting YTHDF2-expressing cells, inhibiting the viability of GSCs without affecting NSCs and impairing in vivo glioblastoma growth. Thus, YTHDF2 links RNA epitranscriptomic modifications and GSC growth, laying the foundation for the YTHDF2-MYC-IGFBP3 axis as a specific and novel therapeutic target in glioblastoma.

2020-09-29 | GSE158740 | GEO

The RNA m6A reader YTHDF2 maintains oncogene expression and is a targetable dependency in glioblastoma stem cells [m6A RIP-seq]

2020-09-29 | GSE158741 | GEO

Identification of novel BMP target genes in glioblastoma

Project description:It has been previously described that in glioblastoma (GBM), BMPs deplete the tumorigenic potential of glioblastoma stem cells (GSCs), promoting their differentiation towards the astrocytic lineage. To gain more insight on how BMPs regulate differentiation in GSCs, we are interested in identifying new BMP target genes in GBM cells. To this end, the patient derived glioblastoma cell lines U3031MG and U3034MG were stimulated or not with 30ng/ml BMP7 for 2 and 24 h, total RNA was isolated from three biological replicates per condition, and a microarray screen with the Affymetrix U133plus2 platform was performed.

2021-05-01 | E-MTAB-9811 | biostudies-arrayexpress

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