Evidence map›Paper›PMID 34404896›Full record

ArticleNPJ precision oncology2021

Clinical, genetic and pharmacological data support targeting the MEK5/ERK5 module in lung cancer.

Adrián Sánchez-Fdez, María Florencia Re-Louhau, Pablo Rodríguez-Núñez, Dolores Ludeña, Sofía Matilla-Almazán, Atanasio Pandiella, Azucena Esparís-Ogando

Abstract read
In one paragraph

Article in NPJ precision oncology, 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
–field-weighted citation impact
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.

  1. Review
  2. MAPK ERK5 is a novel regulator of MHC-I in cancer cells.Cell communication and signaling : CCS · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. ERK5 Interacts with Mitochondrial Glutaminase and Regulates Its Expression.International journal of molecular sciences · 2024
    Article
  9. Actionable Driver Events in Small Cell Lung Cancer.International journal of molecular sciences · 2023
    Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. 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

7 authors.

Adrián Sánchez-FdezInstitute of Molecular and Cellular Biology of Cancer (IBMCC)-CSIC, Salamanca, Spain.
María Florencia Re-LouhauInstitute of Molecular and Cellular Biology of Cancer (IBMCC)-CSIC, Salamanca, Spain.
Pablo Rodríguez-NúñezInstitute of Molecular and Cellular Biology of Cancer (IBMCC)-CSIC, Salamanca, Spain.
Dolores LudeñaInstitute of Biomedical Research of Salamanca (IBSAL), Salamanca, Spain.
Sofía Matilla-AlmazánInstitute of Molecular and Cellular Biology of Cancer (IBMCC)-CSIC, Salamanca, Spain.
Atanasio PandiellaInstitute of Molecular and Cellular Biology of Cancer (IBMCC)-CSIC, Salamanca, Spain.
Azucena Esparís-OgandoInstitute of Molecular and Cellular Biology of Cancer (IBMCC)-CSIC, Salamanca, Spain. esparis@usal.es.ORCID http://orcid.org/0000-0003-4550-4192

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite advances in its treatment, lung cancer still represents the most common and lethal tumor. Because of that, efforts to decipher the pathophysiological actors that may promote lung tumor generation/progression are being made, with the final aim of establishing new therapeutic options. Using a transgenic mouse model, we formerly demonstrated that the sole activation of the MEK5/ERK5 MAPK route had a pathophysiological role in the onset of lung adenocarcinomas. Given the prevalence of that disease and its frequent dismal prognosis, our findings opened the possibility of targeting the MEK5/ERK5 route with therapeutic purposes. Here we have explored such possibility. We found that increased levels of MEK5/ERK5 correlated with poor patient prognosis in lung cancer. Moreover, using genetic as well as pharmacological tools, we show that targeting the MEK5/ERK5 route is therapeutically effective in lung cancer. Not only genetic disruption of ERK5 by CRISPR/Cas9 caused a relevant inhibition of tumor growth in vitro and in vivo; such ERK5 deficit augmented the antitumoral effect of agents normally used in the lung cancer clinic. The clinical correlation studies together with the pharmacological and genetic results establish the basis for considering the targeting of the MEK5/ERK5 route in the therapy for lung cancer.

Identifiers

PMID34404896
PMCPMC8371118

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.