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  1. Article: Doryphagy: when selective autophagy safeguards centrosome integrity.

    Cianfanelli, Valentina / Cecconi, Francesco

    Molecular & cellular oncology

    2020  Volume 7, Issue 2, Page(s) 1719021

    Abstract: Although centrosome abnormalities are frequent in cancer, the mechanisms responsible for their accumulation are poorly understood. Here we comment on our recent publication identifying a new type of selective autophagy, named doryphagy, which preserves ... ...

    Abstract Although centrosome abnormalities are frequent in cancer, the mechanisms responsible for their accumulation are poorly understood. Here we comment on our recent publication identifying a new type of selective autophagy, named doryphagy, which preserves centrosome organization through targeting Centriolar Satellites (CS). Thus, doryphagy prevents inaccurate mitosis and genomic instability.
    Language English
    Publishing date 2020-02-07
    Publishing country United States
    Document type Journal Article
    ISSN 2372-3556
    ISSN 2372-3556
    DOI 10.1080/23723556.2020.1719021
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Editorial: Molecular Mechanisms of Selective Autophagy in Human Disease.

    Cianfanelli, Valentina / Grumati, Paolo / Nazio, Francesca

    Frontiers in cell and developmental biology

    2020  Volume 8, Page(s) 664

    Language English
    Publishing date 2020-08-06
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2020.00664
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Cloud hunting: doryphagy, a form of selective autophagy that degrades centriolar satellites.

    Holdgaard, Søs Grønbæk / Cianfanelli, Valentina / Cecconi, Francesco

    Autophagy

    2019  Volume 16, Issue 2, Page(s) 379–381

    Abstract: The selective clearance of cellular components by macroautophagy (hereafter autophagy) is critical for maintaining cellular homeostasis. In this punctum, we summarize and discuss our recent findings regarding a novel type of selective autophagy that ... ...

    Abstract The selective clearance of cellular components by macroautophagy (hereafter autophagy) is critical for maintaining cellular homeostasis. In this punctum, we summarize and discuss our recent findings regarding a novel type of selective autophagy that targets centriolar satellites (CS) for degradation, a process we termed doryphagy from the Greek word "doryphoros", standing for "satellite". CS are microtubule-associated protein complexes that regulate centrosome composition. We show that CS degradation is mediated through a direct interaction between GABARAPs and an LC3-interacting region (LIR) motif in the CS protein PCM1. Autophagy-deficient systems accumulate large abnormal CS and consequently display centrosome reorganization and abnormal mitoses. Our findings provide a mechanistic link between autophagy deficiency and centrosome abnormalities and exemplify how mammalian Atg8-family proteins (mATG8s) can regulate substrate specificity.
    MeSH term(s) Animals ; Autophagy ; Centrioles/metabolism ; Humans ; Microtubules/metabolism ; Mitosis ; Models, Biological ; Multiprotein Complexes/metabolism ; Proteolysis ; Substrate Specificity
    Chemical Substances Multiprotein Complexes
    Language English
    Publishing date 2019-12-19
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.1080/15548627.2019.1703356
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: AMBRA1: When autophagy meets cell proliferation.

    Cianfanelli, Valentina / Cecconi, Francesco

    Autophagy

    2015  Volume 11, Issue 9, Page(s) 1705–1707

    Abstract: A growing amount of evidence reported in the literature in recent years strongly supports the relevance of the interplay between autophagy and other pathways. In this context, the study of the link between autophagy and cell proliferation regulation has ... ...

    Abstract A growing amount of evidence reported in the literature in recent years strongly supports the relevance of the interplay between autophagy and other pathways. In this context, the study of the link between autophagy and cell proliferation regulation has been among the most challenging. In our recent publications, we finely characterize a role for the pro-autophagic protein AMBRA1 in the regulation of cell proliferation. AMBRA1 modulates autophagy and interacts with PPP2/PP2A (protein phosphatase 2), thus also modulating MYC protein levels and the cell proliferation rate. Interestingly, this pathway of regulation is controlled by the master regulator of autophagy and cell growth, MTORC1. Notably, in our study we demonstrate the relevance of the AMBRA1-mediated regulation of MYC in tumorigenesis, also identifying AMBRA1 as a tumor suppressor gene.
    Language English
    Publishing date 2015
    Publishing country United States
    Document type Comment ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.1080/15548627.2015.1053681
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  5. Article ; Online: Autophagy and cancer stem cells: molecular mechanisms and therapeutic applications.

    Nazio, Francesca / Bordi, Matteo / Cianfanelli, Valentina / Locatelli, Franco / Cecconi, Francesco

    Cell death and differentiation

    2019  Volume 26, Issue 4, Page(s) 690–702

    Abstract: Autophagy and mitophagy act in cancer as bimodal processes, whose differential functions strictly depend on cancer ontogenesis, progression, and type. For instance, they can act to promote cancer progression by helping cancer cells survive stress or, ... ...

    Abstract Autophagy and mitophagy act in cancer as bimodal processes, whose differential functions strictly depend on cancer ontogenesis, progression, and type. For instance, they can act to promote cancer progression by helping cancer cells survive stress or, instead, when mutated or abnormal, to induce carcinogenesis by influencing cell signaling or promoting intracellular toxicity. For this reason, the study of autophagy in cancer is the main focus of many researchers and several clinical trials are already ongoing to manipulate autophagy and by this way determine the outcome of disease therapy. Since the establishment of the cancer stem cell (CSC) theory and the discovery of CSCs in individual cancer types, autophagy and mitophagy have been proposed as key mechanisms in their homeostasis, dismissal or spread, even though we still miss a comprehensive view of how and by which regulatory molecules these two processes drive cell fate. In this review, we will dive into the deep water of autophagy, mitophagy, and CSCs and offer novel viewpoints on possible therapeutic strategies, based on the modulation of these degradative systems.
    MeSH term(s) Animals ; Autophagy/drug effects ; Autophagy/genetics ; Autophagy/immunology ; Humans ; Mitophagy/drug effects ; Mitophagy/genetics ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/therapy ; Neoplastic Stem Cells/cytology ; Neoplastic Stem Cells/drug effects ; Neoplastic Stem Cells/immunology ; Neoplastic Stem Cells/metabolism ; Signal Transduction/drug effects ; Signal Transduction/genetics ; Signal Transduction/immunology ; Tumor Microenvironment/drug effects ; Tumor Microenvironment/genetics ; Tumor Microenvironment/immunology
    Language English
    Publishing date 2019-02-06
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1225672-9
    ISSN 1476-5403 ; 1350-9047
    ISSN (online) 1476-5403
    ISSN 1350-9047
    DOI 10.1038/s41418-019-0292-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 4230: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 80: Show issues

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  6. Article: The Intraflagellar Transport Protein IFT20 Recruits ATG16L1 to Early Endosomes to Promote Autophagosome Formation in T Cells.

    Finetti, Francesca / Cassioli, Chiara / Cianfanelli, Valentina / Zevolini, Fabrizia / Onnis, Anna / Gesualdo, Monica / Brunetti, Jlenia / Cecconi, Francesco / Baldari, Cosima T

    Frontiers in cell and developmental biology

    2021  Volume 9, Page(s) 634003

    Abstract: Lymphocyte homeostasis, activation and differentiation crucially rely on basal autophagy. The fine-tuning of this process depends on autophagy-related (ATG) proteins and their interaction with the trafficking machinery that orchestrates the membrane ... ...

    Abstract Lymphocyte homeostasis, activation and differentiation crucially rely on basal autophagy. The fine-tuning of this process depends on autophagy-related (ATG) proteins and their interaction with the trafficking machinery that orchestrates the membrane rearrangements leading to autophagosome biogenesis. The underlying mechanisms are as yet not fully understood. The intraflagellar transport (IFT) system, known for its role in cargo transport along the axonemal microtubules of the primary cilium, has emerged as a regulator of autophagy in ciliated cells. Growing evidence indicates that ciliogenesis proteins participate in cilia-independent processes, including autophagy, in the non-ciliated T cell. Here we investigate the mechanism by which IFT20, an integral component of the IFT system, regulates basal T cell autophagy. We show that IFT20 interacts with the core autophagy protein ATG16L1 and that its CC domain is essential for its pro-autophagic activity. We demonstrate that IFT20 is required for the association of ATG16L1 with the Golgi complex and early endosomes, both of which have been identified as membrane sources for phagophore elongation. This involves the ability of IFT20 to interact with proteins that are resident at these subcellular localizations, namely the golgin GMAP210 at the Golgi apparatus and Rab5 at early endosomes. GMAP210 depletion, while leading to a dispersion of ATG16L1 from the Golgi, did not affect basal autophagy. Conversely, IFT20 was found to recruit ATG16L1 to early endosomes tagged for autophagosome formation by the BECLIN 1/VPS34/Rab5 complex, which resulted in the local accumulation of LC3. Hence IFT20 participates in autophagosome biogenesis under basal conditions by regulating the localization of ATG16L1 at early endosomes to promote autophagosome biogenesis. These data identify IFT20 as a new regulator of an early step of basal autophagy in T cells.
    Language English
    Publishing date 2021-03-22
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2021.634003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Cell biology: Molecular clearance at the cell's antenna.

    Cianfanelli, Valentina / Cecconi, Francesco

    Nature

    2013  Volume 502, Issue 7470, Page(s) 180–181

    MeSH term(s) Animals ; Autophagy/physiology ; Centrioles/metabolism ; Cilia/physiology ; Humans ; Proteins/metabolism
    Chemical Substances OFD1 protein, mouse ; Proteins
    Language English
    Publishing date 2013-10-02
    Publishing country England
    Document type News ; Comment
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/nature12693
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    Zs.A 26: Show issues Location:
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    Zs.MG 9: Show issues
    Zs.MO 244: Show issues

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  8. Article ; Online: Autophagy-dependent NFκB regulation.

    Cianfanelli, Valentina / Cecconi, Francesco

    Cell cycle (Georgetown, Tex.)

    2012  Volume 11, Issue 3, Page(s) 436–437

    MeSH term(s) Animals ; Autophagy ; Humans ; NF-kappa B/metabolism
    Chemical Substances NF-kappa B
    Language English
    Publishing date 2012-02-01
    Publishing country United States
    Document type News ; Comment
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    DOI 10.4161/cc.11.3.19224
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 5881: Show issues Location:
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  9. Article ; Online: MIR7-3HG, a MYC-dependent modulator of cell proliferation, inhibits autophagy by a regulatory loop involving AMBRA1.

    Capizzi, Mariacristina / Strappazzon, Flavie / Cianfanelli, Valentina / Papaleo, Elena / Cecconi, Francesco

    Autophagy

    2017  Volume 13, Issue 3, Page(s) 554–566

    Abstract: Macroautophagy/autophagy is a tightly regulated intracellular catabolic pathway involving the lysosomal degradation of cytoplasmic organelles and proteins to be recycled into metabolic precursors. AMBRA1 (autophagy and Beclin 1 regulator 1) has a central ...

    Abstract Macroautophagy/autophagy is a tightly regulated intracellular catabolic pathway involving the lysosomal degradation of cytoplasmic organelles and proteins to be recycled into metabolic precursors. AMBRA1 (autophagy and Beclin 1 regulator 1) has a central role in the autophagy signaling network; it acts upstream of MTORC1-dependent autophagy by stabilizing the kinase ULK1 (unc-51 like autophagy activating kinase 1) and by favoring autophagosome core complex formation. AMBRA1 also regulates the cell cycle by modulating the activity of the phosphatase PPP2/PP2A (protein phosphatase 2) and degradation of MYC. Of note, post-transcriptional regulation mediated by noncoding microRNAs (MIRNAs) contributes significantly to control autophagy. Here we describe a new role for the microRNA MIR7-3HG/MIR-7 as a potent autophagy inhibitor. Indeed, MIR7-3HG targets the 3' untranslated region (UTR) of AMBRA1 mRNA, inducing a decrease of both AMBRA1 mRNA and protein levels, and thus causing a block in autophagy. Furthermore, MIR7-3HG, through AMBRA1 downregulation, prevents MYC dephosphorylation, establishing a positive feedback for its own transcription. These data suggest a new and interesting role of MIR7-3HG as an anti-autophagic MIRNA that may affect oncogenesis through the regulation of the tumor suppressor AMBRA1.
    Language English
    Publishing date 2017-03-04
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.1080/15548627.2016.1269989
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: Connecting autophagy: AMBRA1 and its network of regulation.

    Cianfanelli, Valentina / Nazio, Francesca / Cecconi, Francesco

    Molecular & cellular oncology

    2015  Volume 2, Issue 1, Page(s) e970059

    Abstract: During autophagy, a double-membraned vesicle called the autophagosome is responsible for the degradation of long-lived proteins and damaged/old organelles, thus contributing to the maintenance of cellular homeostasis. Physiological stimuli and stressors ... ...

    Abstract During autophagy, a double-membraned vesicle called the autophagosome is responsible for the degradation of long-lived proteins and damaged/old organelles, thus contributing to the maintenance of cellular homeostasis. Physiological stimuli and stressors enhance autophagy in order to accomplish important processes such as cell differentiation or as a cytoprotective response. In line with this, numerous studies have demonstrated the relevance of proper autophagy regulation to health. Autophagy defects are associated with the insurgence of neurological/neurodegenerative diseases and cancer. Moreover, the autophagy pathway is often potentiated in cancer cells to increase cell survival. Increased knowledge of the molecular mechanisms underlying autophagy regulation and their interplay with other cellular pathways would provide advances in cancer treatment. In this context, post-translational modifications, protein-protein interactions, and regulative feedback loops offer promising insights. In this review, we focus on AMBRA1, a proautophagic protein that was recently demonstrated to participate in numerous crucial regulative mechanisms of the autophagy process.
    Language English
    Publishing date 2015-02-24
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 2372-3556
    ISSN 2372-3556
    DOI 10.4161/23723548.2014.970059
    Database MEDical Literature Analysis and Retrieval System OnLINE

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