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Updated: Mar 21, 2026

Analysis of Lymph Node Volume by Ultra-High-Frequency Ultrasound Imaging in the Braf/Pten Genetically Engineered Mouse Model of Melanoma
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Analysis of Lymph Node Volume by Ultra-High-Frequency Ultrasound Imaging in the Braf/Pten Genetically Engineered Mouse Model of Melanoma

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RMEL3, a novel BRAFV600E-associated long noncoding RNA, is required for MAPK and PI3K signaling in melanoma

Lucas Goedert1,2, Cristiano G Pereira1, Jason Roszik3

  • 1Department of Cell and Molecular Biology, Faculty of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, São Paulo, Brazil.

Oncotarget
|May 12, 2016
PubMed

Insights

The long non-coding RNA RMEL3 is highly expressed in melanoma and drives tumor cell growth by activating MAPK and PI3K signaling pathways. Silencing RMEL3 significantly reduces melanoma cell survival and proliferation, offering a potential therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Previous studies identified RMEL3 as a long non-coding RNA (lncRNA) with elevated expression in melanoma.
  • The Cancer Genome Atlas (TCGA) data confirmed RMEL3 enrichment in melanoma and its correlation with the BRAFV600E mutation.

Purpose of the Study:

  • To investigate the functional role of RMEL3 in BRAFV600E melanoma.
  • To elucidate the molecular mechanisms by which RMEL3 influences melanoma cell signaling and proliferation.

Main Methods:

  • Analysis of TCGA data to correlate RMEL3 expression with clinical and molecular features.
  • siRNA-mediated knockdown of RMEL3 in melanoma cell lines.
  • Western blot analysis to assess protein level changes in key signaling pathways.
  • Flow cytometry to analyze cell cycle distribution.

Main Results:

  • RMEL3 knockdown reduced colony formation by 95% in BRAFV600E melanoma cells.
  • RMEL3 knockdown led to downregulation of MAPK and PI3K pathway activators/effectors (FGF2, FGF3, DUSP6, ITGB3, GNG2).
  • Knockdown resulted in increased PTEN, p21, p27 protein levels and decreased pAKT, BRAF, pRB, cyclin B1, causing G1/G0 cell cycle arrest.

Conclusions:

  • RMEL3 is essential for maintaining MAPK and PI3K signaling in BRAFV600E melanoma.
  • RMEL3 knockdown significantly impairs melanoma cell survival and proliferation.
  • RMEL3 represents a potential therapeutic target for melanoma treatment.
Keywords:
ENSG00000250961ENST00000506106.1TCGAlncRNAncRNA

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