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Updated: Jun 16, 2026

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells
06:09

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells

Published on: June 7, 2019

DDERMMAL, a melanocytic long non-coding RNA, confers DNA damage tolerance to melanoma cells

Sara Adnane1, Yvessa Verheyden1, Alessandro Cuomo2

  • 1Laboratory for RNA Cancer Biology, Department of Oncology, KU Leuven, 3001 Leuven, Belgium.

Iscience
|June 15, 2026
PubMed

Insights

This study identifies the long non-coding RNA DDERMMAL as a key player in melanoma drug resistance. DDERMMAL helps melanoma cells survive DNA damage, promoting persistence and relapse.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Melanoma treatment faces challenges due to intrinsic drug resistance and eventual relapse in patients.
  • Genetic and non-genetic mechanisms contribute to the emergence of resistant cancer cell clones under therapy.
  • Understanding drug tolerance and resistance mechanisms is crucial for developing effective melanoma treatments.

Purpose of the Study:

  • To investigate the role of long non-coding RNAs (lncRNAs) in melanoma's DNA damage response (DDR) and therapeutic resistance.
  • To identify novel biomarkers and therapeutic vulnerabilities associated with melanoma persistence and relapse.

Main Methods:

  • Identification and characterization of the lncRNA DDERMMAL in melanoma cells.
  • Analysis of DDERMMAL's function in modulating DNA damage response (DDR) signaling.
  • Assessment of DDERMMAL's impact on melanoma cell proliferation and genetic stability under stress.

Main Results:

  • The lncRNA DDERMMAL was identified as a significant modulator of DNA damage response (DDR) signaling in melanoma.
  • DDERMMAL was found to enable melanoma cells to tolerate genetic insults while maintaining proliferation.
  • This function provides a mechanistic explanation for melanoma cell persistence and the development of new mutations driving relapse.

Conclusions:

  • DDERMMAL plays a critical role in conferring melanoma cells resistance to DNA damage, promoting survival and proliferation.
  • DDERMMAL represents a potential therapeutic target for overcoming drug resistance and preventing relapse in melanoma patients.
  • Further research into lncRNAs like DDERMMAL is essential for advancing melanoma treatment strategies.
Keywords:
Cancer systems biologyCell biology

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