Evidence map›Paper›PMID 34805151›Full record

ArticleFrontiers in cell and developmental biology2021

ERK5 Inhibition Induces Autophagy-Mediated Cancer Cell Death by Activating ER Stress.

Andrés Gámez-García, Idoia Bolinaga-Ayala, Guillermo Yoldi, Sergio Espinosa-Gil, Nora Diéguez-Martínez, Elisabet Megías-Roda, Pau Muñoz-Guardiola, Jose M Lizcano

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. MAPK ERK5 is a novel regulator of MHC-I in cancer cells.Cell communication and signaling : CCS · 2026
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  3. Review
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  17. Autophagy in gastrointestinal cancers.Frontiers in oncology · 2022
    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

8 authors at 2 institutions in 1 country.

Andrés Gámez-GarcíaDepartament de Bioquímica i Biologia Molecular and Institut de Neurociències, Universitat Autònoma de Barcelona (UAB), Barcelona, Spain.
Idoia Bolinaga-AyalaDepartament de Bioquímica i Biologia Molecular and Institut de Neurociències, Universitat Autònoma de Barcelona (UAB), Barcelona, Spain.
Guillermo YoldiDepartament de Bioquímica i Biologia Molecular and Institut de Neurociències, Universitat Autònoma de Barcelona (UAB), Barcelona, Spain.
Sergio Espinosa-GilDepartament de Bioquímica i Biologia Molecular and Institut de Neurociències, Universitat Autònoma de Barcelona (UAB), Barcelona, Spain.
Nora Diéguez-MartínezDepartament de Bioquímica i Biologia Molecular and Institut de Neurociències, Universitat Autònoma de Barcelona (UAB), Barcelona, Spain.
Elisabet Megías-RodaDepartament de Bioquímica i Biologia Molecular and Institut de Neurociències, Universitat Autònoma de Barcelona (UAB), Barcelona, Spain.
Pau Muñoz-GuardiolaDepartament de Bioquímica i Biologia Molecular and Institut de Neurociències, Universitat Autònoma de Barcelona (UAB), Barcelona, Spain.
Jose M LizcanoDepartament de Bioquímica i Biologia Molecular and Institut de Neurociències, Universitat Autònoma de Barcelona (UAB), Barcelona, Spain.
Universitat Autònoma de Barcelona · ESVall d'Hebron Institut de Recerca · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is a highly conserved intracellular process that preserves cellular homeostasis by mediating the lysosomal degradation of virtually any component of the cytoplasm. Autophagy is a key instrument of cellular response to several stresses, including endoplasmic reticulum (ER) stress. Cancer cells have developed high dependency on autophagy to overcome the hostile tumor microenvironment. Thus, pharmacological activation or inhibition of autophagy is emerging as a novel antitumor strategy. ERK5 is a novel member of the MAP kinase family that is activated in response to growth factors and different forms of stress. Recent work has pointed ERK5 as a major player controlling cancer cell proliferation and survival. Therefore small-molecule inhibitors of ERK5 have shown promising therapeutic potential in different cancer models. Here, we report for the first time ERK5 as a negative regulator of autophagy. Thus, ERK5 inhibition or silencing induced autophagy in a panel of human cancer cell lines with different mutation patterns. As reported previously, ERK5 inhibitors (ERK5i) induced apoptotic cancer cell death. Importantly, we found that autophagy mediates the cytotoxic effect of ERK5i, since

Indexed as

antitumor drugapoptosisautopaghycancer cell survivalendoplamic reticulum stressERK5 kinaseMAPK signal pathwayUPR – unfolded protein response

Identifiers

PMID34805151
PMCPMC8600073
OpenAlexW3211642506

What Socratic 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 Socratic graph.