Evidence map›Paper›PMID 30053382›Full record

ArticleTranslational research : the journal of laboratory and clinical medicine2018

MAFG is a potential therapeutic target to restore chemosensitivity in cisplatin-resistant cancer cells by increasing reactive oxygen species.

Olga Vera-Puente, Carlos Rodriguez-Antolin, Ana Salgado-Figueroa, Patrycja Michalska, Olga Pernia, Brett M Reid, RocÍo Rosas, Alvaro Garcia-Guede, Silvia SacristÁn, Julia Jimenez and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Translational research : the journal of laboratory and clinical medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

24 citing papers in PubMed, 35 citations in OpenAlex.

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  17. Advances in Oligonucleotide Aptamers for NSCLC Targeting.International journal of molecular sciences · 2020
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  18. Review
  19. Aptamers in Non-Small Cell Lung Cancer Treatment.Molecules (Basel, Switzerland) · 2020
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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

17 authors at 5 institutions in 2 countries.

Olga Vera-PuenteCancer Epigenetics Laboratory, INGEMM, La Paz University Hospital, Madrid, Spain; Biomarkers and Experimental Therapeutics in Cancer, IdiPAZ, Madrid, Spain.
Carlos Rodriguez-AntolinCancer Epigenetics Laboratory, INGEMM, La Paz University Hospital, Madrid, Spain; Biomarkers and Experimental Therapeutics in Cancer, IdiPAZ, Madrid, Spain.
Ana Salgado-FigueroaDepartment of Biochemistry Research, Laboratory of Aptamers, IRYCIS-Hospital Ramón y Cajal, Madrid, Spain.
Patrycja MichalskaBiomedical Research Foundation of University Hospital La Princesa, Madrid, Spain; Institute Teófilo Hernando and Department of Pharmacology and Therapeutics, Autonomous University of Madrid, Madrid, Spain.
Olga PerniaCancer Epigenetics Laboratory, INGEMM, La Paz University Hospital, Madrid, Spain; Biomarkers and Experimental Therapeutics in Cancer, IdiPAZ, Madrid, Spain.
Brett M ReidDepartment of Cancer Epidemiology, MOFFITT Cancer Center, Tampa, Florida.
RocÍo RosasCancer Epigenetics Laboratory, INGEMM, La Paz University Hospital, Madrid, Spain; Biomarkers and Experimental Therapeutics in Cancer, IdiPAZ, Madrid, Spain.
Alvaro Garcia-GuedeCancer Epigenetics Laboratory, INGEMM, La Paz University Hospital, Madrid, Spain; Biomarkers and Experimental Therapeutics in Cancer, IdiPAZ, Madrid, Spain.
Silvia SacristÁnDepartment of Biochemistry Research, Laboratory of Aptamers, IRYCIS-Hospital Ramón y Cajal, Madrid, Spain.
Julia JimenezBiomarkers and Experimental Therapeutics in Cancer, IdiPAZ, Madrid, Spain.
Isabel Esteban-RodriguezBiomarkers and Experimental Therapeutics in Cancer, IdiPAZ, Madrid, Spain; Department of Pathology, La Paz University Hospital, Madrid, Spain.
M Elena MartinDepartment of Biochemistry Research, Laboratory of Aptamers, IRYCIS-Hospital Ramón y Cajal, Madrid, Spain.
Thomas A SellersDepartment of Cancer Epidemiology, MOFFITT Cancer Center, Tampa, Florida.
Rafael LeónBiomedical Research Foundation of University Hospital La Princesa, Madrid, Spain; Institute Teófilo Hernando and Department of Pharmacology and Therapeutics, Autonomous University of Madrid, Madrid, Spain.
VÍctor M GonzalezDepartment of Biochemistry Research, Laboratory of Aptamers, IRYCIS-Hospital Ramón y Cajal, Madrid, Spain.
Javier De CastroBiomarkers and Experimental Therapeutics in Cancer, IdiPAZ, Madrid, Spain.
Inmaculada Ibanez de CaceresCancer Epigenetics Laboratory, INGEMM, La Paz University Hospital, Madrid, Spain; Biomarkers and Experimental Therapeutics in Cancer, IdiPAZ, Madrid, Spain. Electronic address: inma.ibanezca@salud.madrid.org.
Hospital La Paz Institute for Health Research · ESInstituto Ramón y Cajal de Investigación Sanitaria · ESHospital Universitario La Paz · ESMoffitt Cancer Center · USUniversidad Autónoma de Madrid · ES

Funding

TRANSLATIONAL RESEARCHP30CA076292 · NCI · UNIVERSITY OF SOUTH FLORIDA · PI KENNETH Lynn WRIGHT · 1998 to 2026
$93.5M
NCI NIH HHS P30 CA076292
6 · The paper itself

Abstract

Adjuvant chemotherapy for solid tumors based on platinum-derived compounds such as cisplatin is the treatment of choice in most cases. Cisplatin triggers signaling pathways that lead to cell death, but it also induces changes in tumor cells that modify the therapeutic response, thereby leading to cisplatin resistance. We have recently reported that microRNA-7 is silenced by DNA methylation and is involved in the resistance to platinum in cancer cells through the action of the musculoaponeurotic fibrosarcoma oncogene family, protein G (MAFG). In the present study, we first confirm the miR-7 epigenetic regulation of MAFG in 44 normal- and/or tumor-paired samples in non-small-cell lung cancer (NSCLC). We also provide translational evidence of the role of MAFG and the clinical outcome in NSCLC by the interrogation of two extensive in silico databases of 2019 patients. Moreover, we propose that MAFG-mediated resistance could be conferred due to lower reactive oxygen species production after cisplatin exposure. We developed specifically selected aptamers against MAFG, with high sensitivity to detect the protein at a nuclear level probed by aptacytochemistry and histochemistry analyses. The inhibition of MAFG activity through the action of the specific aptamer apMAFG6F increased the levels of reactive oxygen species production and the sensitivity to cisplatin. We report first the specific nuclear identification of MAFG as a novel detection method for diagnosis in NSCLC, and then we report that MAFG modulates the redox response and confers cell protection against free radicals generated after platinum administration, thus also being a promising therapeutic target.

Indexed as

Aptamers, NucleotideCarcinoma, Non-Small-Cell LungCell Line, TumorCisplatinCloning, MolecularDNA MethylationDrug Resistance, NeoplasmEpigenesis, GeneticGene ExpressionGene SilencingHEK293 CellsHumansLung NeoplasmsMafG Transcription FactorMicroRNAsOxidation-ReductionAptamers, NucleotideCisplatinMAFG protein, humanMafG Transcription FactorMicroRNAsMIRN7-1 microRNA, humanReactive Oxygen SpeciesRepressor Proteins

Identifiers

PMID30053382
PMCPMC7787305
OpenAlexW2810539286

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.