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  Tumor suppression in mice lacking GABARAP, an Atg8/LC3 family member implicated in autophagy, is associated with alterations in cytokine secretion and cell death

Salah, F., Ebbinghaus, M., Muley, V., Zhou, Z., Al-Saadi, K., Pacyna-Gengelbach, M., et al. (2016). Tumor suppression in mice lacking GABARAP, an Atg8/LC3 family member implicated in autophagy, is associated with alterations in cytokine secretion and cell death. Cell Death and Disease, 7: e2205, pp. 1-11. doi:10.1038/cddis.2016.93.

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Item Permalink: https://hdl.handle.net/11858/00-001M-0000-002C-14FB-2 Version Permalink: https://hdl.handle.net/11858/00-001M-0000-002C-151A-3
Genre: Journal Article

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 Creators:
Salah, FS, Author
Ebbinghaus, M, Author
Muley, VY, Author
Zhou, Z, Author
Al-Saadi, KRD, Author
Pacyna-Gengelbach, M, Author
O'Sullivan, GA, Author
Betz, Heinrich1, Author           
König, R, Author
Wang, Z-Q, Author
Bräuer, R, Author
Petersen, I, Author
Affiliations:
1Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society, ou_1497704              

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 Abstract: GABARAP belongs to an evolutionary highly conserved gene family that has a fundamental role in autophagy. There is ample evidence for a crosstalk between autophagy and apoptosis as well as the immune response. However, the molecular details for these interactions are not fully characterized. Here, we report that the ablation of murine GABARAP, a member of the Atg8/LC3 family that is central to autophagosome formation, suppresses the incidence of tumor formation mediated by the carcinogen DMBA and results in an enhancement of the immune response through increased secretion of IL-1β, IL-6, IL-2 and IFN-γ from stimulated macrophages and lymphocytes. In contrast, TGF-β1 was significantly reduced in the serum of these knockout mice. Further, DMBA treatment of these GABARAP knockout mice reduced the cellularity of the spleen and the growth of mammary glands through the induction of apoptosis. Gene expression profiling of mammary glands revealed significantly elevated levels of Xaf1, an apoptotic inducer and tumor-suppressor gene, in knockout mice. Furthermore, DMBA treatment triggered the upregulation of pro-apoptotic (Bid, Apaf1, Bax), cell death (Tnfrsf10b, Ripk1) and cell cycle inhibitor (Cdkn1a, Cdkn2c) genes in the mammary glands. Finally, tumor growth of B16 melanoma cells after subcutaneous inoculation was inhibited in GABARAP-deficient mice. Together, these data provide strong evidence for the involvement of GABARAP in tumorigenesis in vivo by delaying cell death and its associated immune-related response.

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Language(s): eng - English
 Dates: 2016-04-282016-04-28
 Publication Status: Published online
 Pages: 11
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Identifiers: DOI: 10.1038/cddis.2016.93
URI: https://www.ncbi.nlm.nih.gov/pubmed/27124579
URI: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4855672/
 Degree: -

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Title: Cell Death and Disease
Source Genre: Journal
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Publ. Info: London : Nature Pub. Group
Pages: - Volume / Issue: 7 Sequence Number: e2205 Start / End Page: 1 - 11 Identifier: ISSN: 2041-4889