Evidence map›Paper›PMID 34830972›Full record

ArticleCancers2021

Tau Regulates Glioblastoma Progression, 3D Cell Organization, Growth and Migration via the PI3K-AKT Axis.

Alessandra Pagano, Gilles Breuzard, Fabrice Parat, Aurélie Tchoghandjian, Dominique Figarella-Branger, Tiphany Coralie De Bessa, Françoise Garrouste, Alexis Douence, Pascale Barbier, Hervé Kovacic

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.8field-weighted citation impact, top 8% 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, 27 citations in OpenAlex.

  1. Degradation fragments of Tau and type IV collagen as serum biomarkers in patients with recurrent glioblastoma treated with nivolumab and bevacizumab.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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  16. Tau Isoforms: Gaining Insight intoInternational journal of molecular sciences · 2022
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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

10 authors at 2 institutions in 2 countries.

Alessandra PaganoFaculté des Sciences Médicales et Paramédicales, Institut de Neurophysiopathologie (INP), Team 9, UMR 7051, CNRS, Aix Marseille Université, 13005 Marseille, France.
Gilles BreuzardFaculté des Sciences Médicales et Paramédicales, Institut de Neurophysiopathologie (INP), Team 9, UMR 7051, CNRS, Aix Marseille Université, 13005 Marseille, France.ORCID 0000-0001-8178-2080
Fabrice ParatFaculté des Sciences Médicales et Paramédicales, Institut de Neurophysiopathologie (INP), Team 9, UMR 7051, CNRS, Aix Marseille Université, 13005 Marseille, France.
Aurélie TchoghandjianFaculté des Sciences Médicales et Paramédicales, Institut de Neurophysiopathologie (INP), Team 8, UMR 7051, CNRS, Aix Marseille Université, 13005 Marseille, France.
Dominique Figarella-BrangerFaculté des Sciences Médicales et Paramédicales, Institut de Neurophysiopathologie (INP), Team 8, UMR 7051, CNRS, Aix Marseille Université, 13005 Marseille, France.
Tiphany Coralie De BessaLIM 64: Instituto do Coracao (InCor), Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo 05403-090, SP, Brazil.ORCID 0000-0002-5771-259X
Françoise GarrousteFaculté des Sciences Médicales et Paramédicales, Institut de Neurophysiopathologie (INP), Team 9, UMR 7051, CNRS, Aix Marseille Université, 13005 Marseille, France.
Alexis DouenceFaculté des Sciences Médicales et Paramédicales, Institut de Neurophysiopathologie (INP), Team 9, UMR 7051, CNRS, Aix Marseille Université, 13005 Marseille, France.
Pascale BarbierFaculté des Sciences Médicales et Paramédicales, Institut de Neurophysiopathologie (INP), Team 9, UMR 7051, CNRS, Aix Marseille Université, 13005 Marseille, France.ORCID 0000-0002-0622-182X
Hervé KovacicFaculté des Sciences Médicales et Paramédicales, Institut de Neurophysiopathologie (INP), Team 9, UMR 7051, CNRS, Aix Marseille Université, 13005 Marseille, France.ORCID 0000-0001-6509-4210
Centre National de la Recherche Scientifique · FRHospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Microtubule-Associated Protein Tau is expressed in several cancers, including low-grade gliomas and glioblastomas. We have previously shown that Tau is crucial for the 2D motility of several glioblastoma cell lines, including U87-MG cells. Using an RNA interference (shRNA), we tested if Tau contributed to glioblastoma in vivo tumorigenicity and analyzed its function in a 3D model of multicellular spheroids (MCS). Tau depletion significantly increased median mouse survival in an orthotopic glioblastoma xenograft model. This was accompanied by the inhibition of MCS growth and cell evasion, as well as decreased MCS compactness, implying N-cadherin mislocalization. Intracellular Signaling Array analysis revealed a defective activation of the PI3K/AKT pathway in Tau-depleted cells. Such a defect in PI3K/AKT signaling was responsible for reduced MCS growth and cell evasion, as demonstrated by the inhibition of the pathway in control MCS using LY294002 or Perifosine, which did not significantly affect Tau-depleted MCS. Finally, analysis of the glioblastoma TCGA dataset showed a positive correlation between the amount of phosphorylated Akt-Ser473 and the expression of

Indexed as

AktglioblastomaMicrotubule-Associated Protein Tau (MAPT)multicellular spheroidN-cadherinPI3 kinase (PI3K)

Identifiers

PMID34830972
PMCPMC8616151
OpenAlexW3216499108

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.