Evidence map›Paper›PMID 41408466›Full record

ArticleOncogene2026

Identification of Raptor and GLI1 as USP37 substrates highlight its context-specific function in medulloblastoma cells.

Ashutosh Singh, Donghang Cheng, Amanda R Haltom, Yanwen Yang, Tara Dobson, Rashieda Hatcher, Veena Rajaram, Vidya Gopalakrishnan

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncogene, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Ashutosh Singh *Department of Pediatrics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Donghang Cheng *Department of Pediatrics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Amanda R HaltomDepartment of Pediatrics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Yanwen YangDepartment of Pediatrics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Tara DobsonDepartment of Pediatrics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Rashieda HatcherDepartment of Pediatrics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Veena RajaramDivision of Pediatric Pathology and Neuropathology, Department of Pathology, UT Southwestern Medical Center, Dallas, TX, USA.
Vidya GopalakrishnanDepartment of Pediatrics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. vgopalak@mdanderson.org.ORCID http://orcid.org/0000-0002-4448-4698

Funding

Study of a Novel Deubiquitylase in MedulloblastomaR01NS079715 · NINDS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI GOPALAKRISHNAN, VIDYA · 2012 to 2015
$1.4M
Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.) 5R01NS079715NINDS NIH HHS R01 NS079715
6 · The paper itself

Abstract

The USP37 gene encodes a deubiquitylase (DUB), which catalyzes the proteolytic removal of ubiquitin moieties from proteins to modulate their stability, cellular localization or activity. Its expression is downregulated in a subgroup of medulloblastomas driven by constitutive activation of sonic hedgehog (SHH) signaling. Patients with SHH-driven medulloblastomas with elevated expression of the RE1 silencing transcription factor (REST) and reduced expression of USP37 have poor outcomes. In previous studies, we showed sustained proliferation of SHH-medulloblastoma cells due to blockade of terminal cell cycle exit and neuronal differentiation stemming from a failure in USP37-dependent stabilization of its target, the cyclin-dependent kinase inhibitor (CDKI)-p27. This finding suggested a tumor suppressive function for USP37. Interestingly, the current study also uncovered Raptor, a component of the mTORC1 complex, as a novel target of USP37. Under conditions of low-USP37 expression, reduced Raptor stability and mTORC1 activity caused a decline in phosphorylation of 4E-binding protein 1 (4EBP1) and increased its interaction with eukaryotic elongation factor 4E (eIF4E), which is known to inhibit CAP-dependent translation initiation. Surprisingly, a subset of patients with SHH-driven medulloblastomas with elevated expression of USP37 and the Glioma-associated Oncogene 1 (GLI1), also exhibited poor outcomes. Using genetic and biochemical analyses, we showed that USP37-mediated stabilization of GLI1, a terminal effector of SHH signaling, increases pathway activity and upregulates expression of its target oncogene product, CCND1, to drive cell proliferation. These data indicate that USP37 elevation in SHH-driven medulloblastomas has the potential to promote non-canonical activation of SHH signaling. Overall, our findings suggest that USP37 may have context-specific oncogenic and tumor suppressive roles in medulloblastoma cells.

Indexed as

Cerebellar NeoplasmsEndopeptidasesMedulloblastomaRegulatory-Associated Protein of mTORUbiquitin ThiolesteraseZinc Finger Protein GLI1Cell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHedgehog ProteinsHumansMechanistic Target of Rapamycin Complex 1Signal TransductionEndopeptidasesGLI1 protein, humanHedgehog ProteinsMechanistic Target of Rapamycin Complex 1Regulatory-Associated Protein of mTORRPTOR protein, humanSHH protein, humanUbiquitin ThiolesteraseUSP37 protein, humanZinc Finger Protein GLI1

Identifiers

PMID41408466
PMCPMC12815662

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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.