Evidence map›Paper›PMID 33375627›Full record

ArticleCancers2020

TAK1 Inhibitor Enhances the Therapeutic Treatment for Glioblastoma.

Michela Campolo, Marika Lanza, Giovanna Casili, Irene Paterniti, Alessia Filippone, Maria Caffo, Salvatore M Cardali, Ivana Puliafito, Cristina Colarossi, Gabriele Raciti and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.5field-weighted citation impact, top 42% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. NG25 Enhances Anti-Tumor Immunity inOncoTargets and therapy · 2026
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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

12 authors at 1 institution in 2 countries.

Michela CampoloDepartment of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, 98122 Messina, Italy.
Marika LanzaDepartment of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, 98122 Messina, Italy.
Giovanna CasiliDepartment of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, 98122 Messina, Italy.
Irene PaternitiDepartment of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, 98122 Messina, Italy.
Alessia FilipponeDepartment of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, 98122 Messina, Italy.
Maria CaffoDepartment of Biomedical and Dental Sciences and Morpho-Functional Imaging, Unit of Neurosurgery, University of Messina, 98122 Messina, Italy.
Salvatore M CardaliDepartment of Biomedical and Dental Sciences and Morpho-Functional Imaging, Unit of Neurosurgery, University of Messina, 98122 Messina, Italy.
Ivana PuliafitoIstituto Oncologico del Mediterraneo, Via Penninazzo 7, 95029 Viagrande, Italy.
Cristina ColarossiIstituto Oncologico del Mediterraneo, Via Penninazzo 7, 95029 Viagrande, Italy.
Gabriele RacitiIOM Ricerca S.r.l., Via Penninazzo 11, 95029 Viagrande, Italy.
Salvatore CuzzocreaDepartment of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, 98122 Messina, Italy.ORCID 0000-0001-6131-3690
Emanuela EspositoDepartment of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, 98122 Messina, Italy.ORCID 0000-0002-2663-6387
University of Messina · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma (GBM) is a brain tumor characterized by poor therapeutic response and overall survival. Despite relevant progress in conventional treatments represented by the clinical use of temozolomide (TMZ), a combination of approaches might be a possible future direction for treating GBM. Transforming growth factor-beta-activated kinase-1 (TAK1) is an essential component in genotoxic stresses-induced NF-κB-activation and mitogen-activated protein kinase (MAPK)-pathways; however, the role of TAK1 in GBM-chemoresistance remains unknown. This study aimed to verify, in GBM human cell lines, in an in vivo U87-xenograft model and in TMZ-treated-patients, the effect of TAK1 inhibition on the sensitivity of GBM cells to chemotherapy. In vitro model, using GBM cell lines, showed that 5Z-7-oxozeaenol augmented the cytotoxic effects of TMZ, blocking TMZ-induced NF-κB-activation, reducing DNA-damage and enhancing TMZ-induced apoptosis in GMB cell lines. We showed a reduction in tumor burden as well as tumor volume in the xenograft model following the treatment with 5Z-7-oxozaenol associated with TMZ. Our results showed a significant up-regulation in TAK1, p-p38, p-JNK and NF-κB in glioblastoma TMZ-treated-patients and denoted the role of 5Z-7-oxozeaenol in increasing the sensitivity of GBM cells to chemotherapy, proving to be an effective coadjuvant to current GBM chemotherapeutic regimens, suggesting a new option for therapeutic treatment of GBM.

Indexed as

cell linesglioblastomapatientsTAK1temozolomide

Identifiers

PMID33375627
PMCPMC7794959
OpenAlexW3115597021

What OpenQuestion holds

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LicenceCC BY
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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.