Evidence map›Paper›PMID 34073238›Full record

ArticleBiology2021

Silencing of Histone Deacetylase 6 Decreases Cellular Malignancy and Contributes to Primary Cilium Restoration, Epithelial-to-Mesenchymal Transition Reversion, and Autophagy Inhibition in Glioblastoma Cell Lines.

Alejandro Urdiciain, Elena Erausquin, María V Zelaya, Idoya Zazpe, José L Lanciego, Bárbara Meléndez, Juan A Rey, Miguel A Idoate, Natalia A Riobo-Del Galdo, Javier S Castresana

Open access · goldAbstract read
In one paragraph

Article in Biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

13 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Article
  3. Histone Deacetylase 6 (HDAC6) in Ciliopathies: Emerging Insights and Therapeutic Implications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. The Potential of Senescence as a Target for Developing Anticancer Therapy.International journal of molecular sciences · 2023
    Review
  9. Review
  10. Review
  11. Targeting HDAC6 to Overcome Autophagy-Promoted Anti-Cancer Drug Resistance.International journal of molecular sciences · 2022
    Review
  12. The Emerging Role of EVA1A in Different Types of Cancers.International journal of molecular sciences · 2022
    Review
  13. Review
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 5 institutions in 2 countries.

Alejandro UrdiciainDepartment of Biochemistry and Genetics, University of Navarra School of Sciences, 31008 Pamplona, Spain.
Elena ErausquinDepartment of Biochemistry and Genetics, University of Navarra School of Sciences, 31008 Pamplona, Spain.
María V ZelayaDepartment of Pathology, Hospital Complex of Navarra, 31008 Pamplona, Spain.
Idoya ZazpeDepartment of Neurosurgery, Hospital Complex of Navarra, 31008 Pamplona, Spain.
José L LanciegoNeurosciences Division, Center for Applied Medical Research (CIMA), University of Navarra, 31008 Pamplona, Spain.ORCID 0000-0003-2301-5419
Bárbara MeléndezMolecular Pathology Research Unit, Virgen de la Salud Hospital, 45005 Toledo, Spain.
Juan A ReyIdiPaz Research Unit, La Paz University Hospital, 28046 Madrid, Spain.
Miguel A IdoateDepartment of Pathology, University of Navarra Clinic, 31008 Pamplona, Spain.
Natalia A Riobo-Del GaldoSchool of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds LS2 9JT, UK.ORCID 0000-0002-8942-7873
Javier S CastresanaDepartment of Biochemistry and Genetics, University of Navarra School of Sciences, 31008 Pamplona, Spain.ORCID 0000-0002-2373-482X
Universidad de Navarra · ESComplejo Hospitalario de Navarra · ESHospital La Paz Institute for Health Research · ESHospital Virgen de la Salud · ESUniversity of Leeds · GB

Funding

Universidad de Navarra 2018/2021
6 · The paper itself

Abstract

Glioblastoma multiforme, the most common type of malignant brain tumor as well as the most aggressive one, lacks an effective therapy. Glioblastoma presents overexpression of mesenchymal markers Snail, Slug, and N-Cadherin and of the autophagic marker p62. Glioblastoma cell lines also present increased autophagy, overexpression of mesenchymal markers, Shh pathway activation, and lack of primary cilia. In this study, we aimed to evaluate the role of HDAC6 in the pathogenesis of glioblastoma, as HDAC6 is the most overexpressed of all HDACs isoforms in this tumor. We treated glioblastoma cell lines with siHDAC6. HDAC6 silencing inhibited proliferation, migration, and clonogenicity of glioblastoma cell lines. They also reversed the mesenchymal phenotype, decreased autophagy, inhibited Shh pathway, and recovered the expression of primary cilia in glioblastoma cell lines. These results demonstrate that HDAC6 might be a good target for glioblastoma treatment.

Indexed as

autophagyepithelial-to-mesenchymal transitionglioblastomaHDAC6primary ciliumsiRNAsonic hedgehog

Identifiers

PMID34073238
PMCPMC8228543
OpenAlexW3165066237

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.