Evidence map›Paper›PMID 26557664›Full record

ArticleBioMed research international2015

All-Trans Retinoic Acid Induces Proliferation, Survival, and Migration in A549 Lung Cancer Cells by Activating the ERK Signaling Pathway through a Transcription-Independent Mechanism.

Reyna Sara Quintero Barceinas, Alejandro García-Regalado, Elena Aréchaga-Ocampo, Nicolás Villegas-Sepúlveda, Claudia Haydée González-De la Rosa

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

14 citing papers in PubMed, 27 citations in OpenAlex.

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  9. Article
  10. Cadmium induces A549 cell migration and invasion by activating ERK.Experimental and therapeutic medicine · 2019
    Article
  11. Review
  12. Article
  13. Review
  14. Preparation andResearch in pharmaceutical sciences · 2017
    Article
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

5 authors at 3 institutions in 1 country.

Reyna Sara Quintero BarceinasDepartamento de Ciencias Naturales, Universidad Autónoma Metropolitana, Unidad Cuajimalpa, Avenida Vasco de Quiroga 4871, 05348 Colonia Santa Fe Cuajimalpa, DF, Mexico.
Alejandro García-RegaladoFacultad de Enfermería, Universidad Autónoma de San Luis Potosí, Avenida Niño Artillero 130, 78240 Zona Universitaria, SLP, Mexico.
Elena Aréchaga-OcampoDepartamento de Ciencias Naturales, Universidad Autónoma Metropolitana, Unidad Cuajimalpa, Avenida Vasco de Quiroga 4871, 05348 Colonia Santa Fe Cuajimalpa, DF, Mexico.
Nicolás Villegas-SepúlvedaDepartamento de Biomedicina Molecular, Centro de Investigación y de Estudios Avanzados del IPN, Avenida Instituto Politécnico Nacional 2508, 14740 Colonia San Pedro Zacatenco, DF, Mexico.
Claudia Haydée González-De la RosaDepartamento de Ciencias Naturales, Universidad Autónoma Metropolitana, Unidad Cuajimalpa, Avenida Vasco de Quiroga 4871, 05348 Colonia Santa Fe Cuajimalpa, DF, Mexico.
Universidad Autónoma Metropolitana · MXAutonomous University of San Luis Potosí · MXInstituto Politécnico Nacional · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

All-trans retinoic acid (ATRA) has been used as an antineoplastic because of its ability to promote proliferation, inhibition, and differentiation, primarily in leukemia; however, in other types of cancer, such as lung cancer, treatment with ATRA is restricted because not all the patients experience the same results. The ERK signaling pathway is dysregulated in cancer cells, including lung cancer, and this dysregulation promotes proliferation and cell invasion. In this study, we demonstrate that treatment with ATRA can activate the ERK signaling pathway by a transcription-independent mechanism through a signaling cascade that involves RARα and PI3K, promoting growth, survival, and migration in lung cancer cells. Until now, this mechanism was unknown in lung cancer cells. The inhibition of the ERK signaling pathway restores the beneficial effects of ATRA, reduces proliferation, increases apoptosis, and blocks the cell migration process in lung cancer cells. In conclusion, our results suggest that the combination of ATRA with ERK inhibitor in clinical trials for lung cancer is warranted.

Indexed as

Antineoplastic AgentsApoptosisCell DifferentiationCell Line, TumorCell MovementCell ProliferationCell SurvivalHumansLung NeoplasmsMAP Kinase Signaling SystemPhosphatidylinositol 3-KinasesReceptors, Retinoic AcidRetinoic Acid Receptor alphaTranscription, GeneticTretinoinAntineoplastic AgentsPhosphatidylinositol 3-KinasesRARA protein, humanReceptors, Retinoic AcidRetinoic Acid Receptor alphaTretinoin

Identifiers

PMID26557664
PMCPMC4628773
OpenAlexW2107955288

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.