The autophagy GABARAPL1 gene is epigenetically regulated in breast cancer models.

BMC Cancer

Université de Franche-Comté, Laboratoire de Biochimie, EA3922 « Estrogènes, Expression Génique et Pathologies du Système Nerveux Central », SFR IBCT FED4234, UFR Sciences et Techniques, 16 route de Gray, 25030, Besançon Cedex, France.

Published: October 2015

AI Article Synopsis

  • The GABARAP family members play key roles in receptor transport and the autophagy process, with downregulated GABARAPL1 linked to poor prognosis in breast cancer patients.
  • Research utilized qRT-PCR, western blotting, and epigenetic quantification to investigate how epigenetic changes affect GABARAP family expression in breast cancer.
  • Findings indicate that reduced GABARAPL1 expression is associated with DNA methylation and histone deacetylation, suggesting that targeting epigenetic mechanisms and CREB-1 modulation could help in developing treatments for breast cancer.

Article Abstract

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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4609056PMC
http://dx.doi.org/10.1186/s12885-015-1761-4DOI Listing

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