Evidence map›Paper›PMID 19880519›Full record

ArticleThe Journal of biological chemistry2010

Oncogenic BRAFV600E induces expression of neuronal differentiation marker MAP2 in melanoma cells by promoter demethylation and down-regulation of transcription repressor HES1.

Nityanand Maddodi, Kumar M R Bhat, Sulochana Devi, Su-Chun Zhang, Vijayasaradhi Setaluri

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. 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
1.5field-weighted citation impact, top 18% 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, 38 citations in OpenAlex.

  1. Review
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  8. Anticancer properties of phospholipase A2 from Daboia siamensis venom on human skin melanoma cells.The journal of venomous animals and toxins including tropical diseases · 2016
    Article
  9. Article
  10. Article
  11. RAFting the rapids of axon regeneration signaling.Neural regeneration research · 2015
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
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  18. Epigenetic regulation of the calcitonin gene-related peptide gene in trigeminal glia.Cephalalgia : an international journal of headache · 2011
    Article
  19. Article
  20. 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

5 authors at 1 institution in 1 country.

Nityanand MaddodiDepartment of Dermatology, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin 53706, USA.
Kumar M R Bhat
Sulochana Devi
Su-Chun Zhang
Vijayasaradhi Setaluri
University of Wisconsin–Madison · US

Funding

Neural Specification of Embryonic Stem CellsR01NS045926 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI ZHANG, SU-CHUN · 2003 to 2013
$3.5M
Prognostic Significance of Neuronal Differentiation of Cutaneous MelanomaR21CA125091 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI SETALURI, VIJAYASARADHI · 2008 to 2009
$364k
NCI NIH HHS R21 CA125091NCI NIH HHS R21CA125091NINDS NIH HHS R01 NS045926NINDS NIH HHS R01NS045926
6 · The paper itself

Abstract

MAP2 is a neuron-specific microtubule-associated protein that binds and stabilizes dendritic microtubules. Previously, we showed that MAP2 expression is (a) activated in cutaneous primary melanoma and (b) inversely associated with melanoma tumor progression. We also showed that ectopic expression of MAP2 in metastatic melanoma cells inhibits cell growth by inducing mitotic spindle defects and apoptosis. However, molecular mechanisms of regulation of MAP2 gene expression in melanoma are not understood. Here, we show that in melanoma cells MAP2 expression is induced by the demethylating agent 5-aza-2'-cytidine, and MAP2 promoter is progressively methylated during melanoma progression, indicating that epigenetic mechanisms are involved in silencing of MAP2 in melanoma. In support of this, methylation of MAP2 promoter DNA in vitro inhibits its activity. Because MAP2 promoter activity levels in melanoma cell lines also correlated with activating mutation in BRAF, a gene that is highly expressed in neurons, we hypothesized that BRAF signaling is involved in MAP2 expression. We show that hyperactivation of BRAF-MEK signaling activates MAP2 expression in melanoma cells by two independent mechanisms, promoter demethylation or down-regulation of neuronal transcription repressor HES1. Our data suggest that BRAF oncogene levels can regulate melanoma neuronal differentiation and tumor progression.

Indexed as

Gene Expression Regulation, NeoplasticPromoter Regions, GeneticAmino Acid SubstitutionAnimalsAzacitidineBasic Helix-Loop-Helix ProteinsBiomarkersCell DifferentiationCell Line, TumorCpG IslandsDNA MethylationDown-RegulationHomeodomain ProteinsHumansMAP Kinase Signaling SystemMelanomaAzacitidineBasic Helix-Loop-Helix ProteinsBiomarkersBRAF protein, humanHES1 protein, humanHomeodomain ProteinsMAP2 protein, humanMicrotubule-Associated ProteinsMitogen-Activated Protein Kinase KinasesMutant ProteinsProto-Oncogene Proteins B-rafTranscription Factor HES-1

Identifiers

PMID19880519
PMCPMC2804171
OpenAlexW2106300482

What OpenQuestion holds

Textmetadata
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.