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EZH2 Inactivates Primary Cilia to Activate Wnt and Drive Melanoma

Peter K Jackson1

  • 1Baxter Laboratory, Department of Microbiology and Immunology and Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA.

Cancer Cell
|July 11, 2018
PubMed

Insights

Enhancer of Zeste Homolog 2 (EZH2) overexpression in melanoma silences primary cilia genes, leading to Wnt pathway activation and cancer progression. This study reveals primary cilia act as tumor suppressors in melanoma.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • EZH2 is amplified in human melanomas.
  • The role of primary cilia in melanoma progression is not fully understood.

Purpose of the Study:

  • To investigate the function of EZH2 in melanoma.
  • To determine the impact of EZH2 overexpression on primary cilia and downstream signaling pathways.

Main Methods:

  • Analysis of EZH2 amplification in melanoma samples.
  • Investigating the effect of EZH2 overexpression on gene expression related to primary cilia.
  • Assessing Wnt pathway activation in response to EZH2 modulation.

Main Results:

  • EZH2 overexpression leads to the silencing of genes essential for primary cilia formation and function (deciliation).
  • Deciliation induced by EZH2 promotes Wnt pathway activation.
  • This mechanism drives the progression of melanomas with BrafV600E or NrasQ61N mutations.

Conclusions:

  • EZH2 acts as an oncoprotein in melanoma by disrupting primary cilia.
  • Primary cilia function as tumor suppressors in melanoma.
  • Targeting EZH2 or restoring cilia function may offer therapeutic strategies for melanoma.

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