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      MicroRNAs: an emerging player in autophagy

        1 ,   1 , *

      ScienceOpen Research

      ScienceOpen

      Life sciences, MicroRNA, Autophagy, Cancer

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          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Autophagy is an evolutionarily conserved self-digestion process for the quality control of intracellular entities in eukaryotes. In the past few years, mounting evidence indicates that microRNAs (miRNAs)-mediated post-transcriptional regulation of gene expression represents an integral part of the autophagy regulatory network and may have a substantial effect on autophagy-related physiological and pathological conditions including cancer. Herein, we examine some of the molecular mechanisms by which miRNAs manipulate the autophagic machinery to maintain cellular homeostasis and their biological outputs during cancer development. A better understanding of interaction between miRNAs and cellular autophagy may ultimately benefit future cancer diagnostic and anticancer therapeutics.

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          Most cited references 41

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          Autophagosome formation: core machinery and adaptations.

          Eukaryotic cells employ autophagy to degrade damaged or obsolete organelles and proteins. Central to this process is the formation of autophagosomes, double-membrane vesicles responsible for delivering cytoplasmic material to lysosomes. In the past decade many autophagy-related genes, ATG, have been identified that are required for selective and/or nonselective autophagic functions. In all types of autophagy, a core molecular machinery has a critical role in forming sequestering vesicles, the autophagosome, which is the hallmark morphological feature of this dynamic process. Additional components allow autophagy to adapt to the changing needs of the cell.
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            Mitochondria supply membranes for autophagosome biogenesis during starvation.

            Starvation-induced autophagosomes engulf cytosol and/or organelles and deliver them to lysosomes for degradation, thereby resupplying depleted nutrients. Despite advances in understanding the molecular basis of this process, the membrane origin of autophagosomes remains unclear. Here, we demonstrate that, in starved cells, the outer membrane of mitochondria participates in autophagosome biogenesis. The early autophagosomal marker, Atg5, transiently localizes to punctae on mitochondria, followed by the late autophagosomal marker, LC3. The tail-anchor of an outer mitochondrial membrane protein also labels autophagosomes and is sufficient to deliver another outer mitochondrial membrane protein, Fis1, to autophagosomes. The fluorescent lipid NBD-PS (converted to NBD-phosphotidylethanolamine in mitochondria) transfers from mitochondria to autophagosomes. Photobleaching reveals membranes of mitochondria and autophagosomes are transiently shared. Disruption of mitochondria/ER connections by mitofusin2 depletion dramatically impairs starvation-induced autophagy. Mitochondria thus play a central role in starvation-induced autophagy, contributing membrane to autophagosomes. Copyright (c) 2010 Elsevier Inc. All rights reserved.
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              Distinct regulation of autophagic activity by Atg14L and Rubicon associated with Beclin 1-phosphatidylinositol-3-kinase complex.

              Beclin 1, a mammalian autophagy protein that has been implicated in development, tumour suppression, neurodegeneration and cell death, exists in a complex with Vps34, the class III phosphatidylinositol-3-kinase (PI(3)K) that mediates multiple vesicle-trafficking processes including endocytosis and autophagy. However, the precise role of the Beclin 1-Vps34 complex in autophagy regulation remains to be elucidated. Combining mouse genetics and biochemistry, we have identified a large in vivo Beclin 1 complex containing the known proteins Vps34, p150/Vps15 and UVRAG, as well as two newly identified proteins, Atg14L (yeast Atg14-like) and Rubicon (RUN domain and cysteine-rich domain containing, Beclin 1-interacting protein). Characterization of the new proteins revealed that Atg14L enhances Vps34 lipid kinase activity and upregulates autophagy, whereas Rubicon reduces Vps34 activity and downregulates autophagy. We show that Beclin 1 and Atg14L synergistically promote the formation of double-membraned organelles that are associated with Atg5 and Atg12, whereas forced expression of Rubicon results in aberrant late endosomal/lysosomal structures and impaired autophagosome maturation. We hypothesize that by forming distinct protein complexes, Beclin 1 and its binding proteins orchestrate the precise function of the class III PI(3)K in regulating autophagy at multiple steps.
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                Author and article information

                Contributors
                (View ORCID Profile)
                Journal
                SOR-LIFE
                ScienceOpen Research
                ScienceOpen
                2199-1006
                22 December 2014
                : 0 (ID: dfcd3b09-eb66-454f-ae5c-19894f1eb382 )
                : 0
                : 1-7
                Affiliations
                [1 ]Department of Molecular Microbiology and Immunology, University of Southern California, Los Angeles, CA, USA
                Author notes
                [* ]Corresponding author's e-mail address: yongfei.yang@ 123456usc.edu ; chengyu.liang@ 123456usc.edu
                Article
                2327:XE
                10.14293/S2199-1006.1.SOR-LIFE.A181CU.v1
                © 2014 Y. Yang and C. Liang.

                This work has been published open access under Creative Commons Attribution License CC BY 4.0 , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Conditions, terms of use and publishing policy can be found at www.scienceopen.com .

                Page count
                Figures: 1, Tables: 0, References: 61, Pages: 7
                Product
                Categories
                Original article

                Life sciences

                Cancer, Autophagy, microRNA

                Comments

                This is very focused and updated review on a topic that is capturing increasing interest in the scientific community. The manuscript is written in a clear and readable manner. There is only a minor typing error to be corrected at pag. 4, right column as indicated below the ability of tumor cells to survive metabolic stresses and thereof sensitized sensitizes hepatocellular The literature cited covers the most relevant papers, though the authors have failed to cite some review-papers on this same subject. Also, the implications in the biology and therapy of diseases (Conclusion, pag. 5), and in particular of cancer could be expanded. In this respect, I would recommend the authors to refer to the papers listed below. The readers would appreciate to read more about the role of miRNAs in the cross-talk between apoptosis and autophagy and the implications in cancer development and chemoresistance. I am in favor of the publication of this article provided that the Authors address the above issues. 1: Chen Y, Fu LL, Wen X, Liu B, Huang J, Wang JH, Wei YQ. Oncogenic and tumor suppressive roles of microRNAs in apoptosis and autophagy. Apoptosis. 2014 Aug;19(8):1177-89. doi: 10.1007/s10495-014-0999-7. 2: Pan B, Yi J, Song H. MicroRNA-mediated autophagic signaling networks and cancer chemoresistance. Cancer Biother Radiopharm. 2013 Oct;28(8):573-8. doi: 10.1089/cbr.2012.1460. 3: Jing Z, Han W, Sui X, Xie J, Pan H. Interaction of autophagy with microRNAs and their potential therapeutic implications in human cancers. Cancer Lett. 2015 Jan 28;356(2 Pt B):332-8. 4: Titone R, Morani F, Follo C, Vidoni C, Mezzanzanica D, Isidoro C. Epigenetic control of autophagy by microRNAs in ovarian cancer. Biomed Res Int. 2014;2014:343542. doi: 10.1155/2014/343542. 5: Liu B, Wen X, Cheng Y. Survival or death: disequilibrating the oncogenic and tumor suppressive autophagy in cancer. Cell Death Dis. 2013 Oct 31;4:e892. doi: 10.1038/cddis.2013.422.
                2015-03-24 10:20 UTC
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