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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Acetylation, Adaptor Proteins, Signal Transducing, Autophagy, Breast Neoplasms, Cell Line, Tumor, Cyclic AMP Response Element-Binding Protein, DNA Methylation, Epigenomics, Female, Gene Expression Regulation, Neoplastic, Histones, Humans, Lymph Nodes, Microtubule-Associated Proteins, Promoter Regions, Genetic.
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Is the autophagy GABARAPL1 gene epigenetically regulated in breast cancer models? Context: 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.
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Our work strongly suggests that epigenetic inhibitors and CREB-1 modulators may be used in the future to regulate autophagy in breast cancer cells. Final Decision: yes