Journal
EMBO MOLECULAR MEDICINE
Volume 5, Issue 2, Pages 309-325Publisher
WILEY
DOI: 10.1002/emmm.201201546
Keywords
breast cancer; dynamin; huntingtin; migration; polyglutamine
Categories
Funding
- Agence Nationale pour la Recherche - Maladies Rares [ANR-09-BLAN-0080]
- Association pour la Recherche sur le Cancer (ARC) [83188]
- CNRS
- INSERM
- Institut Curie
- Fundacao para a Ciencia e a Tecnologia (FCT, Portugal) [SFRH/BD/60728/2009]
- ARC
- MENRT doctoral fellowship
- INTERFACE Inserm grant
- Agence Nationale de la Recherche (ANR) [ANR-09-BLAN-0080] Funding Source: Agence Nationale de la Recherche (ANR)
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In Huntington disease (HD), polyglutamine expansion in the huntingtin protein causes specific neuronal death. The consequences of the presence of mutant huntingtin in other tissues are less well understood. Here we propose that mutant huntingtin influences breast cancer progression. Indeed, we show that mammary tumours appear earlier in mouse breast cancer models expressing mutant huntingtin as compared to control mice expressing wild-type huntingtin. Tumours bearing mutant huntingtin have a modified gene expression pattern that reflects enhanced aggressiveness with the overexpression of genes favouring invasion and metastasis. In agreement, mutant huntingtin accelerates epithelial to mesenchymal transition and enhances cell motility and invasion. Also, lung metastasis is higher in HD conditions than in control mice. Finally, we report that in HD, the dynamin dependent endocytosis of the ErbB2/HER2 receptor tyrosine kinase is reduced. This leads to its accumulation and to subsequent increases in cell motility and proliferation. Our study may thus have important implications for both cancer and HD.
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