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Omori 2016 Abstract Mito Xmas Meeting Innsbruck

From Bioblast
Exploring the role of mitochondrial dynamics in melanocytes and melanomas.


Omori A, Migliorini D, Scorrano L (2016)

Event: Mito Xmas Meeting 2016 Innsbruck AT

Melanin, the pigment that colors the skin, hair and eyes, is made by cells called melanocytes. Melanin serves multiple purposes, one of which is skin protection against UV irradiation [1]. However, melanocytes can become origins of melanoma, the most aggressive type of skin cancer with high mortality. Despite recent advances in cancer research, there are only few effective treatments for melanoma. It has been shown that aging symptoms, such as hair graying, are caused by defective self-maintenance of melanocyte stem cells (MSC). In fact, Bcl2 deficiency causes selective apoptosis in the MSC and accelerates hair graying. The anti-apoptotic Bcl2 protein suppresses cytochrome c release from mitochondrial cristae [2,3]. These reports suggest that mitochondria play important roles for melanocyte/MSC survival.

Mitochondrial fission and fusion (mitochondrial dynamics) play critical roles in maintaining functional mitochondria. Mitochondrial dynamics are regulated by ubiquitously expressed Dynamin-related GTPases. Dynamin related protein1 mediates fission, while Mitofusin 1 and 2 in the outer mitochondrial membrane and Optic atrophy (Opa1) mediate fusion. However, the involvement of mitochondrial dynamics on melanocyte regulation and growth of melanoma is poorly known.

Despite the well-known role of Bcl2, the anti apoptotic role of Opa1, which keeps cristae structures tight and suppresses cytochrome c release, is less well established in melanocytes and melanoma. Remarkably, we found a significant increase of Opa1 in several cancer melanoma cell lines. We also observed the gray hair syndrome in melanocyte specific Opa1 mutants. These data suggest important functions of Opa1 in melanocytes and highlights a new potential therapeutic target for melanoma.

Labels: MiParea: mt-Structure;fission;fusion  Pathology: Cancer 

Event: A1, Oral 


Omori A(1,2), Migliorini D(1), Scorrano L(1,2)
  1. Dept Biochem, Univ Padova, Italy
  2. VIMM, Venetian Inst Mol Med, Padova, Italy