Evidence map›Paper›PMID 27462428›Full record

ArticleCell discovery2015

Increased CD271 expression by the NF-kB pathway promotes melanoma cell survival and drives acquired resistance to BRAF inhibitor vemurafenib.

Abdelali Lehraiki, Michael Cerezo, Florian Rouaud, Patricia Abbe, Marilyne Allegra, Jerome Kluza, Philippe Marchetti, Veronique Imbert, Yann Cheli, Corine Bertolotto and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell discovery, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

47 citing papers in PubMed, 69 citations in OpenAlex.

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  10. Pharmaceuticals (Basel, Switzerland) · 2023
    Article
  11. Review
  12. Article
  13. Article
  14. Tracking of Melanoma Cell Plasticity by Transcriptional Reporters.International journal of molecular sciences · 2022
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. ATF-3 expression inhibits melanoma growth by downregulating ERK and AKT pathways.Laboratory investigation; a journal of technical methods and pathology · 2021
    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

12 authors at 4 institutions in 1 country.

Abdelali LehraikiINSERM, U1065, équipe 1, Centre Méditerranéen de Médecine Moléculaire (C3M), Nice, France; Université de Nice Sophia Antipolis, UFR de Médecine, Nice, France.
Michael CerezoINSERM, U1065, équipe 1, Centre Méditerranéen de Médecine Moléculaire (C3M), Nice, France; Université de Nice Sophia Antipolis, UFR de Médecine, Nice, France.
Florian RouaudINSERM, U1065, équipe 1, Centre Méditerranéen de Médecine Moléculaire (C3M), Nice, France; Université de Nice Sophia Antipolis, UFR de Médecine, Nice, France.
Patricia AbbeINSERM, U1065, équipe 1, Centre Méditerranéen de Médecine Moléculaire (C3M), Nice, France; Université de Nice Sophia Antipolis, UFR de Médecine, Nice, France.
Marilyne AllegraINSERM, U1065, équipe 1, Centre Méditerranéen de Médecine Moléculaire (C3M), Nice, France; Université de Nice Sophia Antipolis, UFR de Médecine, Nice, France.
Jerome KluzaINSERM, U837, équipe 4 et Faculté de Médecine, Université de Lille II , Lille, France.
Philippe MarchettiINSERM, U837, équipe 4 et Faculté de Médecine, Université de Lille II , Lille, France.
Veronique ImbertINSERM, U1065, équipe 4, Centre Méditerranéen de Médecine Moléculaire (C3M) , Nice, France.
Yann CheliINSERM, U1065, équipe 1, Centre Méditerranéen de Médecine Moléculaire (C3M), Nice, France; Université de Nice Sophia Antipolis, UFR de Médecine, Nice, France.
Corine BertolottoINSERM, U1065, équipe 1, Centre Méditerranéen de Médecine Moléculaire (C3M), Nice, France; Université de Nice Sophia Antipolis, UFR de Médecine, Nice, France; Service de Dermatologie, Hôpital Archet II, CHU, Nice, France.
Robert BallottiINSERM, U1065, équipe 1, Centre Méditerranéen de Médecine Moléculaire (C3M), Nice, France; Université de Nice Sophia Antipolis, UFR de Médecine, Nice, France; Service de Dermatologie, Hôpital Archet II, CHU, Nice, France.
Stéphane RocchiINSERM, U1065, équipe 1, Centre Méditerranéen de Médecine Moléculaire (C3M), Nice, France; Université de Nice Sophia Antipolis, UFR de Médecine, Nice, France; Service de Dermatologie, Hôpital Archet II, CHU, Nice, France.
Centre Méditerranéen de Médecine Moléculaire · FRInserm · FRUniversité de Lille · FRUniversité Côte d'Azur · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Specific BRAFV600E inhibitors (BRAFi) are highly effective in the treatment of melanoma. However, acquired drug resistances invariably develop after the initial response. Therefore, the identification of new mechanisms of acquired resistance gives important clues towards the development of therapies that could elicit long lasting responses. Here we report that CD271 confers resistance to BRAFi in melanoma cells. The expression of CD271 is increased by BRAFi through a stimulation of tumor necrosis factor-alpha (TNFα) secretion that leads to NF-κB signaling pathway activation. CD271 is upregulated in a subset of BRAFi-resistant melanoma cells. The inhibition of TNFα/NF-κB pathway and CD271 silencing restore the BRAFi sensitivity of resistant melanoma cells. Finally, increase of CD271 expression is validated in BRAFi-resistant xenografts tumors and also in tumors from the patients who relapsed under BRAFi. In summary, these results reveal a novel TNFα/NF-κB/CD271 axis whose activation contributes to the acquisition of resistance to BRAFi and therefore may represent a novel therapeutic target to improve the efficacy of therapy in melanoma.

Indexed as

CD271melanomaNF-κBresistanceTNFαvemurafenib

Identifiers

PMID27462428
PMCPMC4860830
OpenAlexW2512420471

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.