Evidence map›Paper›PMID 37443071›Full record

ArticleCell death & disease2023

Targeting Wnt/β-catenin-mediated upregulation of oncogenic NLGN3 suppresses cancer stem cells in glioblastoma.

Eun-Jin Yun, Donghwi Kim, Sangwoo Kim, Jer-Tsong Hsieh, Seung Tae Baek

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
10.3field-weighted citation impact, top 1% of its field
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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

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  6. Recent advances in molecular mechanisms of microRNAs in pathogenesis and resistance of treatment in glioblastoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 3 countries.

Eun-Jin YunPOSTECH Biotech Center, POSTECH, Pohang, Republic of Korea.ORCID 0000-0002-4454-7150
Donghwi KimDepartment of Life Sciences, POSTECH, Pohang, Republic of Korea.
Sangwoo KimDepartment of Biomedical Systems Informatics and Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Republic of Korea.ORCID 0000-0001-5356-0827
Jer-Tsong HsiehDepartment of Biotechnology, Kaohsiung Medical University, Kaohsiung, Taiwan, Republic of China.ORCID 0000-0002-1919-6010
Seung Tae BaekDepartment of Life Sciences, POSTECH, Pohang, Republic of Korea. sbaek@postech.ac.kr.ORCID 0000-0003-0040-1501
Pohang University of Science and Technology · KRKaohsiung Medical University · TWYonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma (GBM) is the most malignant tumor in brain and is highly resistant to therapy. Clinical evidence suggests increased number of cancer stem cells (CSCs) may contribute to the failure of conventional therapies, but the mechanisms associated with acquisition of CSC properties in GBM are not fully understood. We found that DAB2IP suppresses CSC properties by targeting the synaptic proteins neuroligin 3 (NLGN3) in GBM. Furthermore, we showed that GBM-derived NLGN3 has an oncogenic function by inducing CSC properties within GBM. Moreover, elevated NLGN3 transcription mediated by Wnt/β-catenin signaling pathway resulted in increased secretion of NLGN3 into the surrounding tumor microenvironment. Both condition media containing NLGN3 and recombinant NLGN3 transformed neighboring cells to CSCs, suggesting NLGN3 as a critical component inducing CSC properties. Furthermore, targeting NLGN3-bearing CSCs using upstream Wnt/β-catenin inhibitors synergistically enhances the efficacy of conventional treatment. Hence, we unveiled the series of regulatory mechanisms for acquisition of CSC properties in GBM progression by Wnt/β-catenin-mediated NLGN3. These results may provide a new targeting strategy to improve the therapeutic efficacy of GBM treatments.

Indexed as

Glioblastomabeta CateninCell Adhesion Molecules, NeuronalCell Line, TumorCell ProliferationHumansMembrane ProteinsNeoplastic Stem CellsNerve Tissue Proteinsras GTPase-Activating ProteinsTumor MicroenvironmentUp-RegulationWnt Signaling Pathwaybeta CateninCell Adhesion Molecules, NeuronalDAB2IP protein, humanMembrane ProteinsNerve Tissue Proteinsneuroligin 3ras GTPase-Activating Proteins

Identifiers

PMID37443071
PMCPMC10344874
OpenAlexW4384154292

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.