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The autophagy GABARAPL1 gene is epigenetically regulated in breast cancer models

BACKGROUND: The GABARAP family members (GABARAP, GABARAPL1/GEC1 and GABARAPL2 /GATE-16) are involved in the intracellular transport of receptors and the autophagy pathway. We previously reported that GABARAPL1 expression was frequently downregulated in cancer cells while a high GABARAPL1 expression...

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Detalles Bibliográficos
Autores principales: Hervouet, Eric, Claude-Taupin, Aurore, Gauthier, Thierry, Perez, Valérie, Fraichard, Annick, Adami, Pascale, Despouy, Gilles, Monnien, Franck, Algros, Marie-Paule, Jouvenot, Michèle, Delage-Mourroux, Régis, Boyer-Guittaut, Michaël
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4609056/
https://www.ncbi.nlm.nih.gov/pubmed/26474850
http://dx.doi.org/10.1186/s12885-015-1761-4
Descripción
Sumario:BACKGROUND: The GABARAP family members (GABARAP, GABARAPL1/GEC1 and GABARAPL2 /GATE-16) are involved in the intracellular transport of receptors and the autophagy pathway. We previously reported that GABARAPL1 expression was frequently downregulated in cancer cells while a high GABARAPL1 expression is a good prognosis marker for patients with lymph node-positive breast cancer. METHODS: In this study, we asked using qRT-PCR, western blotting and epigenetic quantification whether the expression of the GABARAP family was regulated in breast cancer by epigenetic modifications. RESULTS: Our data demonstrated that a specific decrease of GABARAPL1 expression in breast cancers was associated with both DNA methylation and histone deacetylation and that CREB-1 recruitment on GABARAPL1 promoter was required for GABARAPL1 expression. CONCLUSIONS: Our work strongly suggests that epigenetic inhibitors and CREB-1 modulators may be used in the future to regulate autophagy in breast cancer cells. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12885-015-1761-4) contains supplementary material, which is available to authorized users.