ArticleCell cycle (Georgetown, Tex.)2012
The BRAF(V600E) causes widespread alterations in gene methylation in the genome of melanoma cells.
Article in Cell cycle (Georgetown, Tex.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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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.
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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.
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Who cites it
54 citing papers in PubMed, 88 citations in OpenAlex.
- Phase II trial of vorinostat in advanced melanoma.Investigational new drugs · 2014Trial
- Advances in Understanding Drug Resistance Mechanisms and Innovative Clinical Treatments for Melanoma.Current treatment options in oncology · 2024Review
- Epigenome Reprogramming Through H3K27 and H3K4 Trimethylation as a Resistance Mechanism to DNA Methylation Inhibition in BRAFV600E-Mutated Colorectal Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
- UHRF1/UBE2L6/UBR4-mediated ubiquitination regulates EZH2 abundance and thereby melanocytic differentiation phenotypes in melanoma.Oncogene · 2023Article
- Combination of BMI1 and MAPK/ERK inhibitors is effective in medulloblastoma.Neuro-oncology · 2022Article
- Drugging the Epigenome: Overcoming Resistance to Targeted and Immunotherapies in Melanoma.JID innovations : skin science from molecules to population health · 2022Review
- Methylation Markers in Cutaneous Melanoma: Unravelling the Potential Utility of Their Tracking by Liquid Biopsy.Cancers · 2021Review
- DNA methyltransferase inhibitors combination therapy for the treatment of solid tumor: mechanism and clinical application.Clinical epigenetics · 2021Review
- H3K27me3-mediated PGC1α gene silencing promotes melanoma invasion through WNT5A and YAP.The Journal of clinical investigation · 2020Article
- Role of VEGFR-1 in melanoma acquired resistance to the BRAF inhibitor vemurafenib.Journal of cellular and molecular medicine · 2020Article
- Second Diagnostic Opinion by Experienced Dermatopathologists in the Setting of a Referral Regional Melanoma Unit Significantly Improves the Clinical Management of Patients With Cutaneous Melanoma.Frontiers in medicine · 2020Article
- Identification of lncRNA-mRNA Regulatory Module to Explore the Pathogenesis and Prognosis of Melanoma.Frontiers in cell and developmental biology · 2020Article
- Extracellular Vesicles and Epigenetic Modifications Are Hallmarks of Melanoma Progression.International journal of molecular sciences · 2019Review
- Quantitative Interrogation of the Human Kinome Perturbed by Two BRAF Inhibitors.Journal of proteome research · 2019Article
- Demethylation by low-dose 5-aza-2'-deoxycytidine impairs 3D melanoma invasion partially through miR-199a-3p expression revealing the role of this miR in melanoma.Clinical epigenetics · 2019Article
- Loss of DNA methylation is related to increased expression of miR-21 and miR-146b in papillary thyroid carcinoma.Clinical epigenetics · 2018Article
- Reversal of Resistance in Targeted Therapy of Metastatic Melanoma: Lessons Learned from Vemurafenib (BRAFCancers · 2018Review
- Co-targeting BET and MEK as salvage therapy for MAPK and checkpoint inhibitor-resistant melanoma.EMBO molecular medicine · 2018Article
- Molecular Mechanisms Governing the Stem Cell's Fate in Brain Cancer: Factors of Stemness and Quiescence.Frontiers in cellular neuroscience · 2018Review
- Oncogenic BRAF mutation induces DNA methylation changes in a murine model for human serrated colorectal neoplasia.Epigenetics · 2018Article
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4 authors at 2 institutions in 2 countries.
Funding
Abstract
Although BRAF(V600E) is well known to play an important role in the tumorigenesis of melanoma, its molecular mechanism, particularly the epigenetic aspect, has been incompletely understood. Here, we investigated the role of BRAF(V600E) signaling in altering gene methylation in the genome of melanoma cells using a methylated CpG island amplification/CpG island microarray system and searched for genes coupled to the BRAF(V600E) signaling through methylation aberrations. The results indicated that a wide range of genes with broad functions were linked to BRAF(V600E) signaling through their hyper- or hypomethylation. Expression of 59 genes hypermethylated upon BRAF knockdown was selectively tested and found to be largely correspondingly underexpressed, suggesting that these genes were naturally hypomethylated, and overexpressed with BRAF(V600E) in melanoma. This BRAF(V600E)-promoted hypomethylation was confirmed on genes selectively examined in primary melanoma tumors. Some of these genes were functionally tested and demonstrated to play a role in melanoma cell proliferation and invasion. As a mechanism of aberrant gene methylation driven by BRAF(V600E), expression of the DNA methyltransferase 1 and histone methyltransferase EZH2 was profoundly affected by BRAF(V600E). We have thus uncovered a previously unrecognized prominent epigenetic mechanism in the tumorigenesis of melanoma driven by BRAF(V600E). Many of the functionally important genes controlled by the BRAF(V600E) signaling through aberrant methylation may prove to be novel therapeutic targets for melanoma.
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Registered trials
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.