Evidence map›Paper›PMID 40770117›Full record

ArticleEMBO molecular medicine2025

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

Hanhee Jo, Sarah Munoz, Aneesh Dalvi, Wenqi Yang, Elizabeth Morozova, Stacey M Glasgow

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in EMBO molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors.

Hanhee Jo *Neurobiology Department, School of Biological Sciences, University of California San Diego, La Jolla, 92093, CA, USA.ORCID http://orcid.org/0000-0002-7964-6650
Sarah Munoz *Neurobiology Department, School of Biological Sciences, University of California San Diego, La Jolla, 92093, CA, USA.ORCID http://orcid.org/0009-0000-3672-8237
Aneesh DalviNeurobiology Department, School of Biological Sciences, University of California San Diego, La Jolla, 92093, CA, USA.ORCID http://orcid.org/0009-0005-0643-5261
Wenqi YangNeurobiology Department, School of Biological Sciences, University of California San Diego, La Jolla, 92093, CA, USA.
Elizabeth MorozovaNeurobiology Department, School of Biological Sciences, University of California San Diego, La Jolla, 92093, CA, USA.
Stacey M GlasgowNeurobiology Department, School of Biological Sciences, University of California San Diego, La Jolla, 92093, CA, USA. sglasgow@ucsd.edu.ORCID http://orcid.org/0000-0003-2716-4948

Funding

Defining transcriptional networks and chromatin conformations regulating glioma tumorigenesisR01NS123385 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GLASGOW, STACEY MARIE · 2021 to 2025
$2.0M
Hellman Foundation (The Hellman Foundation) n/aHHS | NIH | National Institute of Neurological Disorders and Stroke (NINDS) 1R01NS123385NINDS NIH HHS R01 NS123385
6 · The paper itself

Abstract

Glioblastoma Multiforme (GBM) is a highly malignant brain cancer with limited effective therapies. 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. We demonstrate that CRIPSR-Cas9 mediated NUAK2 deletion in GBM cells results in suppression of proliferation, while overexpression leads to enhanced cell growth 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.

Indexed as

Brain NeoplasmsGlioblastomaProtein Serine-Threonine KinasesAnimalsBrainCell Line, TumorCell MovementCell ProliferationHumansMiceOncogenesProtein Serine-Threonine KinasesExtracellular MatrixFetal OncogeneGlioblastomaNeurodevelopmentNUAK2

Identifiers

PMID40770117
PMCPMC12423323

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.