Evidence map›Paper›PMID 30209685›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2019

SOX3 can promote the malignant behavior of glioblastoma cells.

Jelena Marjanovic Vicentic, Danijela Drakulic, Idoia Garcia, Vladanka Vukovic, Paula Aldaz, Nela Puskas, Igor Nikolic, Goran Tasic, Savo Raicevic, Laura Garros-Regulez and 5 more

Abstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.3field-weighted citation impact, top 23% 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

22 citing papers in PubMed, 36 citations in OpenAlex.

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  7. Crosstalk betweenInternational journal of molecular sciences · 2023
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  14. The Role of Neurodevelopmental Pathways in Brain Tumors.Frontiers in cell and developmental biology · 2021
    Review
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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

15 authors at 6 institutions in 4 countries.

Jelena Marjanovic VicenticLaboratory for Human Molecular Genetics, Institute of Molecular Genetics and Genetic Engineering, University of Belgrade, Belgrade, Serbia.
Danijela DrakulicLaboratory for Human Molecular Genetics, Institute of Molecular Genetics and Genetic Engineering, University of Belgrade, Belgrade, Serbia. danijeladrakulic@imgge.bg.ac.rs.ORCID http://orcid.org/0000-0001-6790-6673
Idoia GarciaCellular Oncology Group, Biodonostia Health Research Institute, San Sebastian, Spain.
Vladanka VukovicLaboratory for Human Molecular Genetics, Institute of Molecular Genetics and Genetic Engineering, University of Belgrade, Belgrade, Serbia.
Paula AldazCellular Oncology Group, Biodonostia Health Research Institute, San Sebastian, Spain.
Nela PuskasInstitute of Histology and Embryology "Aleksandar Ð. Kostić", School of Medicine, University of Belgrade, Belgrade, Serbia.
Igor NikolicClinical Center of Serbia, Clinic for Neurosurgery, Belgrade, Serbia.
Goran TasicClinical Center of Serbia, Clinic for Neurosurgery, Belgrade, Serbia.
Savo RaicevicClinical Center of Serbia, Clinic for Neurosurgery, Belgrade, Serbia.
Laura Garros-RegulezCellular Oncology Group, Biodonostia Health Research Institute, San Sebastian, Spain.
Nicolas SampronCellular Oncology Group, Biodonostia Health Research Institute, San Sebastian, Spain.
Michael J AtkinsonInstitute of Radiation Biology, Helmholtz Center Munich, German Research Center for Environmental Health, Neuherberg, Germany.
Natasa AnastasovInstitute of Radiation Biology, Helmholtz Center Munich, German Research Center for Environmental Health, Neuherberg, Germany.
Ander MatheuCellular Oncology Group, Biodonostia Health Research Institute, San Sebastian, Spain.
Milena StevanovicLaboratory for Human Molecular Genetics, Institute of Molecular Genetics and Genetic Engineering, University of Belgrade, Belgrade, Serbia.
University of Belgrade · RSBiogipuzkoa Health Research Institute · ESHelmholtz Zentrum München · DEIkerbasque · ESCentar za Promociju Nauke · RSSerbian Academy of Sciences and Arts · RS

Funding

Ministry of Education, Science and Technological Development, Republic of Serbia 173051Serbian Academy of Sciences and Arts F24
6 · The paper itself

Abstract

purposeGlioblastoma is the most common and lethal adult brain tumor. Despite current therapeutic strategies, including surgery, radiation and chemotherapy, the median survival of glioblastoma patients is 15 months. The development of this tumor depends on a sub-population of glioblastoma stem cells governing tumor propagation and therapy resistance. SOX3 plays a role in both normal neural development and carcinogenesis. However, little is known about its role in glioblastoma. Thus, the aim of this work was to elucidate the role of SOX3 in glioblastoma.

methodsSOX3 expression was assessed using real-time quantitative PCR (RT-qPCR), Western blotting and immunohistochemistry. MTT, immunocytochemistry and Transwell assays were used to evaluate the effects of exogenous SOX3 overexpression on the viability, proliferation, migration and invasion of glioblastoma cells, respectively. The expression of Hedgehog signaling pathway components and autophagy markers was assessed using RT-qPCR and Western blot analyses, respectively.

resultsHigher levels of SOX3 expression were detected in a subset of primary glioblastoma samples compared to those in non-tumoral brain tissues. Exogenous overexpression of this gene was found to increase the proliferation, viability, migration and invasion of glioblastoma cells. We also found that SOX3 up-regulation was accompanied by an enhanced activity of the Hedgehog signaling pathway and by suppression of autophagy in glioblastoma cells. Additionally, we found that SOX3 expression was elevated in patient-derived glioblastoma stem cells, as well as in oncospheres derived from glioblastoma cell lines, compared to their differentiated counterparts, implying that SOX3 expression is associated with the undifferentiated state of glioblastoma cells.

conclusionFrom our data we conclude that SOX3 can promote the malignant behavior of glioblastoma cells.

Indexed as

AdultAgedAged, 80 and overAutophagyBrain NeoplasmsCell Line, TumorCell MovementCell ProliferationCell SurvivalFemaleGene Expression Regulation, NeoplasticGlioblastomaHedgehog ProteinsHumansMaleMiddle AgedHedgehog ProteinsSOX3 protein, humanSOXB1 Transcription FactorsTemozolomideAutophagyGlioblastomaGlioblastoma stem cellsHedgehog signalingMigrationSOX3

Identifiers

PMID30209685
PMCPMC12994348
OpenAlexW2891212741

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.