Evidence map›Paper›PMID 34655447›Full record

ArticleJournal of cellular and molecular medicine2021

ERK5 signalling pathway is a novel target of sorafenib: Implication in EGF biology.

Marta Ortega-Muelas, Olga Roche, Diego M Fernández-Aroca, José A Encinar, David Albandea-Rodríguez, Elena Arconada-Luque, Raquel Pascual-Serra, Ismael Muñoz, Isabel Sánchez-Pérez, Borja Belandia and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. VCAN Is Essential for ERK5-Driven Tumorigenesis in Soft Tissue Sarcoma.International journal of biological sciences · 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 4 institutions in 1 country.

Marta Ortega-MuelasLaboratorio de Oncología Molecular, Unidad de Medicina Molecular, Centro Regional de Investigaciones Biomédicas Universidad de Castilla-La Mancha, Unidad Asociada de Biomedicina UCLM, Unidad asociada al CSIC, Albacete, Spain.
Olga RocheLaboratorio de Oncología Molecular, Unidad de Medicina Molecular, Centro Regional de Investigaciones Biomédicas Universidad de Castilla-La Mancha, Unidad Asociada de Biomedicina UCLM, Unidad asociada al CSIC, Albacete, Spain.
Diego M Fernández-ArocaLaboratorio de Oncología Molecular, Unidad de Medicina Molecular, Centro Regional de Investigaciones Biomédicas Universidad de Castilla-La Mancha, Unidad Asociada de Biomedicina UCLM, Unidad asociada al CSIC, Albacete, Spain.
José A EncinarInstituto de Investigación, Desarrollo e Innovación en Biotecnología de Elche (IDiBE) e Instituto de Biología Molecular y Celular (IBMC), Universidad Miguel Hernández (UMH), Elche, Spain.
David Albandea-RodríguezDepartamento de Biología del Cáncer, Instituto de Investigaciones Biomédicas 'Alberto Sols' (CSIC-UAM), Unidad asociada de Biomedicina UCLM, Unidad asociada al CSIC, Madrid, Spain.
Elena Arconada-LuqueLaboratorio de Oncología Molecular, Unidad de Medicina Molecular, Centro Regional de Investigaciones Biomédicas Universidad de Castilla-La Mancha, Unidad Asociada de Biomedicina UCLM, Unidad asociada al CSIC, Albacete, Spain.
Raquel Pascual-SerraLaboratorio de Oncología Molecular, Unidad de Medicina Molecular, Centro Regional de Investigaciones Biomédicas Universidad de Castilla-La Mancha, Unidad Asociada de Biomedicina UCLM, Unidad asociada al CSIC, Albacete, Spain.
Ismael MuñozDepartamento de Biología del Cáncer, Instituto de Investigaciones Biomédicas 'Alberto Sols' (CSIC-UAM), Unidad asociada de Biomedicina UCLM, Unidad asociada al CSIC, Madrid, Spain.
Isabel Sánchez-PérezDepartamento de Bioquímica, Facultad de Medicina, Instituto de Investigaciones Biomédicas 'Alberto Sols' (CSIC-UAM), Unidad asociada de Biomedicina UCLM, Unidad asociada al CSIC, Madrid, Spain.
Borja BelandiaDepartamento de Biología del Cáncer, Instituto de Investigaciones Biomédicas 'Alberto Sols' (CSIC-UAM), Unidad asociada de Biomedicina UCLM, Unidad asociada al CSIC, Madrid, Spain.
María J Ruiz-HidalgoLaboratorio de Oncología Molecular, Unidad de Medicina Molecular, Centro Regional de Investigaciones Biomédicas Universidad de Castilla-La Mancha, Unidad Asociada de Biomedicina UCLM, Unidad asociada al CSIC, Albacete, Spain.
Ricardo Sánchez-PrietoLaboratorio de Oncología Molecular, Unidad de Medicina Molecular, Centro Regional de Investigaciones Biomédicas Universidad de Castilla-La Mancha, Unidad Asociada de Biomedicina UCLM, Unidad asociada al CSIC, Albacete, Spain.ORCID 0000-0003-0882-9780
University of Castilla-La Mancha · ESInstituto de Investigaciones Biomédicas Sols-Morreale · ESConsejo Superior de Investigaciones Científicas · ESUniversitat de Miguel Hernández d'Elx · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sorafenib is a multikinase inhibitor widely used in cancer therapy with an antitumour effect related to biological processes as proliferation, migration or invasion, among others. Initially designed as a Raf inhibitor, Sorafenib was later shown to also block key molecules in tumour progression such as VEGFR and PDGFR. In addition, sorafenib has been connected with key signalling pathways in cancer such as EGFR/EGF. However, no definitive clue about the molecular mechanism linking sorafenib and EGF signalling pathway has been established so far. Our data in HeLa, U2OS, A549 and HEK293T cells, based on in silico, chemical and genetic approaches demonstrate that the MEK5/ERK5 signalling pathway is a novel target of sorafenib. In addition, our data show how sorafenib is able to block MEK5-dependent phosphorylation of ERK5 in the Ser218/Tyr220, affecting the transcriptional activation associated with ERK5. Moreover, we demonstrate that some of the effects of this kinase inhibitor onto EGF biological responses, such as progression through cell cycle or migration, are mediated through the effect exerted onto ERK5 signalling pathway. Therefore, our observations describe a novel target of sorafenib, the ERK5 signalling pathway, and establish new mechanistic insights for the antitumour effect of this multikinase inhibitor.

Indexed as

Biomarkers, TumorCell CycleCell Line, TumorCell MovementDisease SusceptibilityEpidermal Growth FactorFlow CytometryHumansMAP Kinase Signaling SystemMitogen-Activated Protein Kinase 7Molecular Targeted TherapyProtein Kinase InhibitorsSignal TransductionSorafenibStructure-Activity RelationshipBiomarkers, TumorEpidermal Growth FactorMAPK7 protein, humanMitogen-Activated Protein Kinase 7Protein Kinase InhibitorsSorafenibEGFERK5MEK5Sorafenib

Identifiers

PMID34655447
PMCPMC8581332
OpenAlexW3206477885

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.