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MYSM1/2A-DUB is an epigenetic regulator in human melanoma and contributes to tumor cell growth

Christina Wilms1, Carsten M Kroeger1, Adelheid V Hainzl1

  • 1Department of Dermatology and Allergic Diseases, Ulm University, 89081 Ulm, Germany.

Oncotarget
|October 6, 2017
PubMed

Insights

The histone H2A deubiquitinase MYSM1 is upregulated in melanoma and drives tumor growth by epigenetically regulating genes like c-MET. Silencing MYSM1 reduces melanoma cell survival and proliferation, identifying it as a potential therapeutic target.

Area of Science:

  • Epigenetics
  • Cancer Biology
  • Molecular Oncology

Background:

  • Histone modifying enzymes, including histone deacetylases (HDACs) and polycomb repressive complex (PRC) components, are crucial in cancer development.
  • The histone H2A deubiquitinase 2A-DUB/Mysm1 (MYSM1) plays a role in hematopoiesis and tissue differentiation by influencing DNA-damage responses.
  • Alterations in MYSM1 have been observed in skin pigmentation and melanocyte specification, suggesting a potential role in melanoma.

Purpose of the Study:

  • To investigate the role of MYSM1 in melanoma formation and progression.
  • To determine if MYSM1 expression is altered in human melanoma samples and cell lines.
  • To evaluate the therapeutic potential of targeting MYSM1 in melanoma.

Main Methods:

  • Analysis of MYSM1 expression in human melanoma samples, nevi, and normal skin.
  • Detection of MYSM1 mRNA and protein levels in melanoma cell lines and murine skin.
  • Induction of MYSM1 expression by growth factors and UVB exposure.
  • Stable silencing of MYSM1 using lentivirally-mediated shRNA in melanoma cells.
  • Assessment of cell survival, proliferation, and soft agar colony formation in MYSM1-silenced cells.
  • Chromatin immunoprecipitation (ChIP) to identify MYSM1 binding sites, such as the c-MET promoter.

Main Results:

  • MYSM1 expression is significantly increased in human melanoma tissues compared to normal skin and nevi.
  • MYSM1 is expressed at mRNA and protein levels in melanoma cell lines and murine skin, inducible by growth factors and UVB.
  • Silencing MYSM1 in melanoma cells markedly reduces their survival and proliferation.
  • MYSM1-silenced cells exhibit reduced proliferation in soft agar assays.
  • MYSM1 was found to bind to the c-MET promoter region in melanoma cells.

Conclusions:

  • MYSM1 is an epigenetic regulator involved in melanoma cell growth and survival.
  • Increased MYSM1 expression is a feature of melanoma.
  • MYSM1 represents a promising novel therapeutic target for melanoma treatment.
Keywords:
UV-radiationepigeneticsmelanomapigmentationtranscriptional regulation

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