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  1. Article ; Online: Lysosomal lipid peroxidation mediates immunogenic cell death.

    Phadatare, Pravin / Debnath, Jayanta

    The Journal of clinical investigation

    2023  Volume 133, Issue 8

    Abstract: Cancer cells rely on lysosome-dependent degradation to recycle nutrients that serve their energetic and biosynthetic needs. Despite great interest in repurposing the antimalarial hydroxychloroquine as a lysosomal inhibitor in clinical oncology trials, ... ...

    Abstract Cancer cells rely on lysosome-dependent degradation to recycle nutrients that serve their energetic and biosynthetic needs. Despite great interest in repurposing the antimalarial hydroxychloroquine as a lysosomal inhibitor in clinical oncology trials, the mechanisms by which hydroxychloroquine and other lysosomal inhibitors induce tumor-cell cytotoxicity remain unclear. In this issue of the JCI, Bhardwaj et al. demonstrate that DC661, a dimeric form of chloroquine that inhibits palmitoyl-protein thioesterase 1 (PPT1), promoted lysosomal lipid peroxidation, resulting in lysosomal membrane permeabilization and tumor cell death. Remarkably, this lysosomal cell death pathway elicited cell-intrinsic immunogenicity and promoted T lymphocyte-mediated tumor cell clearance. The findings provide the mechanistic foundation for the potential combined use of immunotherapy and lysosomal inhibition in clinical trials.
    MeSH term(s) Humans ; Hydroxychloroquine/metabolism ; Lipid Peroxidation ; Immunogenic Cell Death ; Chloroquine/pharmacology ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Lysosomes/metabolism
    Chemical Substances Hydroxychloroquine (4QWG6N8QKH) ; Chloroquine (886U3H6UFF)
    Language English
    Publishing date 2023-04-17
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Comment
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI169240
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  2. Article ; Online: Secretory autophagy during lysosome inhibition (SALI).

    Debnath, Jayanta / Leidal, Andrew M

    Autophagy

    2022  Volume 18, Issue 10, Page(s) 2498–2499

    Abstract: Both macroautophagy/autophagy and extracellular vesicle (EV) secretion pathways converge upon the endolysosome system. Although lysosome impairment leads to defects in autophagic degradation, the impact of such dysfunction on EV secretion remains poorly ... ...

    Abstract Both macroautophagy/autophagy and extracellular vesicle (EV) secretion pathways converge upon the endolysosome system. Although lysosome impairment leads to defects in autophagic degradation, the impact of such dysfunction on EV secretion remains poorly understood. Recently, we uncovered a novel secretory autophagy pathway that employs EVs and nanoparticles (EVPs) for the secretion of autophagy cargo receptors outside the cell when either autophagosome maturation or lysosomal function is blocked. We term this process secretory autophagy during lysosome inhibition (SALI). SALI functionally requires multiple steps in classical autophagosome formation and the small GTPase RAB27A. Because the intracellular accumulation of autophagy cargo receptors perturbs cell signaling and quality control pathways, we propose that SALI functions as a failsafe mechanism to preserve protein and cellular homeostasis when autophagic or lysosomal degradation is impaired.
    MeSH term(s) Autophagy/physiology ; Endosomes/metabolism ; Lysosomes/metabolism ; Monomeric GTP-Binding Proteins/metabolism ; Secretory Pathway
    Chemical Substances Monomeric GTP-Binding Proteins (EC 3.6.5.2)
    Language English
    Publishing date 2022-07-14
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.1080/15548627.2022.2095788
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  3. Article ; Online: Autophagy and autophagy-related pathways in cancer.

    Debnath, Jayanta / Gammoh, Noor / Ryan, Kevin M

    Nature reviews. Molecular cell biology

    2023  Volume 24, Issue 8, Page(s) 560–575

    Abstract: Maintenance of protein homeostasis and organelle integrity and function is critical for cellular homeostasis and cell viability. Autophagy is the principal mechanism that mediates the delivery of various cellular cargoes to lysosomes for degradation and ... ...

    Abstract Maintenance of protein homeostasis and organelle integrity and function is critical for cellular homeostasis and cell viability. Autophagy is the principal mechanism that mediates the delivery of various cellular cargoes to lysosomes for degradation and recycling. A myriad of studies demonstrate important protective roles for autophagy against disease. However, in cancer, seemingly opposing roles of autophagy are observed in the prevention of early tumour development versus the maintenance and metabolic adaptation of established and metastasizing tumours. Recent studies have addressed not only the tumour cell intrinsic functions of autophagy, but also the roles of autophagy in the tumour microenvironment and associated immune cells. In addition, various autophagy-related pathways have been described, which are distinct from classical autophagy, that utilize parts of the autophagic machinery and can potentially contribute to malignant disease. Growing evidence on how autophagy and related processes affect cancer development and progression has helped guide efforts to design anticancer treatments based on inhibition or promotion of autophagy. In this Review, we discuss and dissect these different functions of autophagy and autophagy-related processes during tumour development, maintenance and progression. We outline recent findings regarding the role of these processes in both the tumour cells and the tumour microenvironment and describe advances in therapy aimed at autophagy processes in cancer.
    MeSH term(s) Humans ; Neoplasms/pathology ; Autophagy/physiology ; Lysosomes ; Tumor Microenvironment
    Language English
    Publishing date 2023-03-02
    Publishing country England
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't
    ZDB-ID 2031313-5
    ISSN 1471-0080 ; 1471-0072
    ISSN (online) 1471-0080
    ISSN 1471-0072
    DOI 10.1038/s41580-023-00585-z
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    Zs.MG 26: Show issues

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  4. Article ; Online: Emerging roles for the autophagy machinery in extracellular vesicle biogenesis and secretion.

    Leidal, Andrew M / Debnath, Jayanta

    FASEB bioAdvances

    2021  Volume 3, Issue 5, Page(s) 377–386

    Abstract: Autophagy classically functions to maintain cell health during stressful conditions by targeting cytosolic components for degradation and recycling via lysosomal pathways. However, accumulating evidence also supports roles for autophagy-related genes ( ... ...

    Abstract Autophagy classically functions to maintain cell health during stressful conditions by targeting cytosolic components for degradation and recycling via lysosomal pathways. However, accumulating evidence also supports roles for autophagy-related genes (ATGs) in non-degradative processes including cellular secretion. Here, we review emerging roles for the autophagy machinery in regulating extracellular vesicle loading and secretion and discuss how functional coupling of these pathways may impact normal physiology and disease.
    Language English
    Publishing date 2021-03-02
    Publishing country United States
    Document type Journal Article
    ISSN 2573-9832
    ISSN (online) 2573-9832
    DOI 10.1096/fba.2020-00138
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  5. Article ; Online: NRF2 activates macropinocytosis upon autophagy inhibition.

    Mondal, Gourish / Debnath, Jayanta

    Cancer cell

    2021  Volume 39, Issue 5, Page(s) 596–598

    Abstract: Su et al. demonstrate that upon inhibiting autophagy, an intracellular nutrient recycling pathway, pancreatic ductal adenocarcinoma cells upregulate NRF2-mediated transcription of macropinocytosis pathway components, thereby triggering an alternate route ...

    Abstract Su et al. demonstrate that upon inhibiting autophagy, an intracellular nutrient recycling pathway, pancreatic ductal adenocarcinoma cells upregulate NRF2-mediated transcription of macropinocytosis pathway components, thereby triggering an alternate route for tumors to scavenge nutrients from extracellular sources. Accordingly, the combined inhibition of autophagy and macropinocytosis may improve cancer treatment.
    MeSH term(s) Autophagy ; Carcinoma, Pancreatic Ductal/drug therapy ; Carcinoma, Pancreatic Ductal/genetics ; Humans ; NF-E2-Related Factor 2/genetics ; Pancreatic Neoplasms/drug therapy ; Pancreatic Neoplasms/genetics ; Pinocytosis
    Chemical Substances NF-E2-Related Factor 2
    Language English
    Publishing date 2021-05-10
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2078448-X
    ISSN 1878-3686 ; 1535-6108
    ISSN (online) 1878-3686
    ISSN 1535-6108
    DOI 10.1016/j.ccell.2021.03.011
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    Zs.A 5650: Show issues Location:
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    Zs.MG 104: Show issues

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  6. Article ; Online: Autophagy in host stromal fibroblasts supports tumor desmoplasia.

    Rudnick, Jenny A / Debnath, Jayanta

    Autophagy

    2021  Volume 17, Issue 12, Page(s) 4497–4498

    Abstract: Growing evidence demonstrates that macroautophagy/autophagy in the host stroma influences the tumor microenvironment. We have uncovered that autophagy in host stromal fibroblasts is compulsory to initiate and maintain the desmoplastic fibrotic response ... ...

    Abstract Growing evidence demonstrates that macroautophagy/autophagy in the host stroma influences the tumor microenvironment. We have uncovered that autophagy in host stromal fibroblasts is compulsory to initiate and maintain the desmoplastic fibrotic response that fosters mammary tumor progression. Genetic loss of fibroblast autophagy impedes COL1A/type 1 collagen secretion, which is required for the development of a stiff tissue matrix permissive for mammary tumor growth. As a result, stromal fibroblast autophagy deficiency impairs mammary tumor progression
    MeSH term(s) Autophagy ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Female ; Fibroblasts/metabolism ; Humans ; Stromal Cells/metabolism ; Tumor Microenvironment
    Language English
    Publishing date 2021-09-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.1080/15548627.2021.1972405
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  7. Article ; Online: Unraveling the mechanisms that specify molecules for secretion in extracellular vesicles.

    Leidal, Andrew M / Debnath, Jayanta

    Methods (San Diego, Calif.)

    2020  Volume 177, Page(s) 15–26

    Abstract: Extracellular vesicles (EVs) are small membrane-bound organelles naturally released from cells and potentially function as vehicles of intercellular communication. Cells release numerous sub-species of EVs, including exosomes and microvesicles, which are ...

    Abstract Extracellular vesicles (EVs) are small membrane-bound organelles naturally released from cells and potentially function as vehicles of intercellular communication. Cells release numerous sub-species of EVs, including exosomes and microvesicles, which are formed via distinct cellular pathways and molecular machineries and contain specific proteins, RNAs and lipids. Accumulating evidence indicates that the repertoire of molecules packaged into EVs is shaped by both the physiological state of the cell and the EV biogenesis pathway involved. Although these observations intimate that precisely regulated pathways sort molecules into EVs, the underlying molecular mechanisms that direct molecules for secretion remain poorly defined. Recently, with the advancement of mass spectrometry, next-generation sequencing techniques and molecular biology tools, several mechanisms contributing to EV cargo selection are beginning to be unraveled. This review examines strategies employed to reveal how specific proteins, RNAs and lipids are directed for secretion via EVs.
    MeSH term(s) Arrestins/genetics ; Arrestins/metabolism ; Cell Communication ; Endosomal Sorting Complexes Required for Transport/genetics ; Endosomal Sorting Complexes Required for Transport/metabolism ; Extracellular Vesicles/chemistry ; Extracellular Vesicles/genetics ; Extracellular Vesicles/metabolism ; Extracellular Vesicles/transplantation ; Gene Expression ; High-Throughput Nucleotide Sequencing/methods ; Humans ; Lipids/chemistry ; Lipids/isolation & purification ; Mass Spectrometry/methods ; Neoplasms/diagnosis ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/therapy ; Neurodegenerative Diseases/diagnosis ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/metabolism ; Neurodegenerative Diseases/therapy ; Organelle Biogenesis ; Protein Interaction Mapping/methods ; RNA/genetics ; RNA/isolation & purification ; RNA/metabolism ; Two-Hybrid System Techniques
    Chemical Substances ARRDC1 protein, human ; Arrestins ; Endosomal Sorting Complexes Required for Transport ; Lipids ; RNA (63231-63-0)
    Language English
    Publishing date 2020-01-21
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1066584-5
    ISSN 1095-9130 ; 1046-2023
    ISSN (online) 1095-9130
    ISSN 1046-2023
    DOI 10.1016/j.ymeth.2020.01.008
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  8. Article ; Online: Unconventional secretion: cargo channeling by TMED10.

    Nguyen, Tan A / Debnath, Jayanta

    Cell research

    2020  Volume 30, Issue 9, Page(s) 713–714

    MeSH term(s) Bodily Secretions/metabolism ; Protein Transport ; Vesicular Transport Proteins/metabolism
    Chemical Substances Vesicular Transport Proteins
    Keywords covid19
    Language English
    Publishing date 2020-07-30
    Publishing country England
    Document type Journal Article ; Comment
    ZDB-ID 1319303-x
    ISSN 1748-7838 ; 1001-0602
    ISSN (online) 1748-7838
    ISSN 1001-0602
    DOI 10.1038/s41422-020-0382-x
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  9. Article ; Online: LC3-dependent extracellular vesicle loading and secretion (LDELS).

    Leidal, Andrew M / Debnath, Jayanta

    Autophagy

    2020  Volume 16, Issue 6, Page(s) 1162–1163

    Abstract: Accumulating evidence implicates various autophagy-related (ATG) proteins in cellular secretion. Recently, we identified a new secretory autophagy pathway in which components of LC3 conjugation machinery specify the incorporation of RNA binding proteins ( ...

    Abstract Accumulating evidence implicates various autophagy-related (ATG) proteins in cellular secretion. Recently, we identified a new secretory autophagy pathway in which components of LC3 conjugation machinery specify the incorporation of RNA binding proteins (RBPs) and small non-coding RNAs into extracellular vesicles (EVs), resulting in their secretion outside of cells. We term this process
    MeSH term(s) Autophagy ; Biological Transport ; Extracellular Vesicles/metabolism ; RNA-Binding Proteins/metabolism
    Chemical Substances RNA-Binding Proteins
    Language English
    Publishing date 2020-04-24
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Comment
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.1080/15548627.2020.1756557
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  10. Article ; Online: Autophagy suppresses breast cancer metastasis by degrading NBR1.

    Marsh, Timothy / Debnath, Jayanta

    Autophagy

    2020  Volume 16, Issue 6, Page(s) 1164–1165

    Abstract: Macroautophagy/autophagy plays complex, context-dependent roles in cancer. How autophagy governs the emergence of metastatic disease has been incompletely understood. We recently uncovered that genetic autophagy inhibition strongly attenuates primary ... ...

    Abstract Macroautophagy/autophagy plays complex, context-dependent roles in cancer. How autophagy governs the emergence of metastatic disease has been incompletely understood. We recently uncovered that genetic autophagy inhibition strongly attenuates primary tumor growth in mammary cancer models, yet paradoxically promotes spontaneous metastasis to the lung and enables the outgrowth of disseminated tumor cells (DTCs) into overt macro-metastases. Furthermore, at both primary and metastatic sites, genetic autophagy inhibition leads to the marked expansion of tumor cells exhibiting aggressive and pro-metastatic basal epithelial differentiation. These pro-metastatic effects of autophagy inhibition are due to the cytosolic accumulation of the autophagy cargo receptor NBR1 in autophagy-deficient tumor cells.
    MeSH term(s) Autophagy ; Breast Neoplasms ; Carrier Proteins ; Humans ; Intracellular Signaling Peptides and Proteins ; Macroautophagy
    Chemical Substances Carrier Proteins ; Intracellular Signaling Peptides and Proteins ; NBR1 protein, human
    Language English
    Publishing date 2020-04-14
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.1080/15548627.2020.1753001
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