Evidence map›Paper›PMID 32555626›Full record

ArticlePloS one2020

miR-410-3p is induced by vemurafenib via ER stress and contributes to resistance to BRAF inhibitor in melanoma.

Tomasz M Grzywa, Klaudia Klicka, Wiktor Paskal, Julia Dudkiewicz, Jarosław Wejman, Michał Pyzlak, Paweł K Włodarski

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Cell Death Modalities in Therapy of Melanoma.International journal of molecular sciences · 2025
    Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. 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

7 authors at 2 institutions in 1 country.

Tomasz M GrzywaDepartment of Methodology, Laboratory of Centre for Preclinical Research, Medical University of Warsaw, Warsaw, Poland.ORCID 0000-0002-1809-248X
Klaudia KlickaDepartment of Methodology, Laboratory of Centre for Preclinical Research, Medical University of Warsaw, Warsaw, Poland.
Wiktor PaskalDepartment of Methodology, Laboratory of Centre for Preclinical Research, Medical University of Warsaw, Warsaw, Poland.ORCID 0000-0003-3051-5446
Julia DudkiewiczDepartment of Methodology, Laboratory of Centre for Preclinical Research, Medical University of Warsaw, Warsaw, Poland.
Jarosław WejmanDepartment of Pathology, Medical Center of Postgraduate Education, Warsaw, Poland.
Michał PyzlakDepartment of Pathology, Medical Center of Postgraduate Education, Warsaw, Poland.
Paweł K WłodarskiDepartment of Methodology, Laboratory of Centre for Preclinical Research, Medical University of Warsaw, Warsaw, Poland.
Medical University of Warsaw · PLPostgraduate School of Molecular Medicine · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite significant development of melanoma therapies, death rates remain high. MicroRNAs, controlling posttranscriptionally gene expression, play role in development of resistance to BRAF inhibitors. The aim of the study was to assess the role of miR-410-3p in response to vemurafenib-BRAF inhibitor. FFPE tissue samples of 12 primary nodular melanomas were analyzed. With the use of Laser Capture Microdissection, parts of tumor, transient tissue, and adjacent healthy tissue were separated. In vitro experiments were conducted on human melanoma cell lines A375, G361, and SK-MEL1. IC50s of vemurafenib were determined using MTT method. Cells were transfected with miR-410-3p mimic, anti-miR-410-3p and their non-targeting controls. ER stress was induced by thapsigargin. Expression of isolated RNA was determined using qRT-PCR. We have found miR-410-3p is downregulated in melanoma tissues. Its expression is induced by vemurafenib in melanoma cells. Upregulation of miR-410-3p level increased melanoma cells resistance to vemurafenib, while its inhibition led to the decrease of resistance. Induction of ER stress increased the level of miR-410-3p. miR-410-3p upregulated the expression of AXL in vitro and correlated with markers of invasive phenotype in starBase. The study shows a novel mechanism of melanoma resistance. miR-410-3p is induced by vemurafenib in melanoma cells via ER stress. It drives switching to the invasive phenotype that leads to the response and resistance to BRAF inhibition.

Indexed as

Cell Line, TumorDown-RegulationDrug Resistance, NeoplasmEndoplasmic Reticulum StressHumansMelanomaMicroRNAsProtein Kinase InhibitorsProto-Oncogene Proteins B-rafVemurafenibMicroRNAsMIRN410 microRNA, humanProtein Kinase InhibitorsProto-Oncogene Proteins B-rafVemurafenib

Identifiers

PMID32555626
PMCPMC7299409
OpenAlexW3036639865

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.