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01.12.2015 | Research article | Ausgabe 1/2015 Open Access

BMC Cancer 1/2015

The autophagy GABARAPL1 gene is epigenetically regulated in breast cancer models

BMC Cancer > Ausgabe 1/2015
Eric Hervouet, Aurore Claude-Taupin, Thierry Gauthier, Valérie Perez, Annick Fraichard, Pascale Adami, Gilles Despouy, Franck Monnien, Marie-Paule Algros, Michèle Jouvenot, Régis Delage-Mourroux, Michaël Boyer-Guittaut
Wichtige Hinweise

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.

Competing interest

The authors declare that they have no competing interests

Authors’ contributions

EH, ACT, TG, VP carried out the molecular studies. FM and MPA participated in the selection of samples and their validation. EH and MBG wrote the manuscript. AF, PA, GD and RDM helped draft the manuscript. All authors have read and approved the final version of the manuscript



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.


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.


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.


Our work strongly suggests that epigenetic inhibitors and CREB-1 modulators may be used in the future to regulate autophagy in breast cancer cells.
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