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  1. Article ; Online: Self-Digestion for Lifespan Extension: Enhanced Autophagy Delays Aging.

    Arensman, Michael D / Eng, Christina H

    Molecular cell

    2018  Volume 71, Issue 4, Page(s) 485–486

    Abstract: By systemically boosting autophagy with a knockin mutation that prevents binding of beclin 1 to BCL2, Fernández et al. (2018) demonstrate that enhanced autophagy prolongs lifespan in mammals. ...

    Abstract By systemically boosting autophagy with a knockin mutation that prevents binding of beclin 1 to BCL2, Fernández et al. (2018) demonstrate that enhanced autophagy prolongs lifespan in mammals.
    MeSH term(s) Animals ; Autophagy ; Beclin-1 ; Longevity ; Mice ; Mutation ; Proto-Oncogene Proteins c-bcl-2
    Chemical Substances Beclin-1 ; Proto-Oncogene Proteins c-bcl-2
    Language English
    Publishing date 2018-08-17
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 1415236-8
    ISSN 1097-4164 ; 1097-2765
    ISSN (online) 1097-4164
    ISSN 1097-2765
    DOI 10.1016/j.molcel.2018.08.002
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    Zs.A 5055: Show issues Location:
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  2. Article ; Online: Revisiting autophagy addiction of tumor cells.

    Nyfeler, Beat / Eng, Christina H

    Autophagy

    2016  Volume 12, Issue 7, Page(s) 1206–1207

    Abstract: Inhibition of autophagy has been widely explored as a potential therapeutic intervention for cancer. Different factors such as tumor origin, tumor stage and genetic background can define a tumor's response to autophagy modulation. Notably, tumors with ... ...

    Abstract Inhibition of autophagy has been widely explored as a potential therapeutic intervention for cancer. Different factors such as tumor origin, tumor stage and genetic background can define a tumor's response to autophagy modulation. Notably, tumors with oncogenic mutations in KRAS were reported to depend on macroautophagy in order to cope with oncogene-induced metabolic stress. Our recent report details the unexpected finding that autophagy is dispensable for KRAS-driven tumor growth in vitro and in vivo. Additionally, we clarify that the antitumorigenic effects of chloroquine, a frequently used nonspecific inhibitor of autophagy, are not connected to the inhibition of macroautophagy. Our data suggest that caution should be exercised when using chloroquine and its analogs to decipher the roles of autophagy in cancer.
    MeSH term(s) Animals ; Antirheumatic Agents/pharmacology ; Autophagy/drug effects ; Cell Line, Tumor ; Chloroquine/pharmacology ; Humans ; Proto-Oncogene Proteins p21(ras)/metabolism
    Chemical Substances Antirheumatic Agents ; KRAS protein, human ; Chloroquine (886U3H6UFF) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
    Language English
    Publishing date 2016-04-20
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.1080/15548627.2016.1170265
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  3. Article ; Online: A metabolic (re-)balancing act.

    Abraham, Robert T / Eng, Christina H

    Molecular cell

    2010  Volume 38, Issue 4, Page(s) 481–482

    Abstract: Cells lacking a functional tuberous sclerosis complex (TSC) heterodimer are sensitized to glucose starvation-induced death. In this issue of Molecular Cell, Choo et al. (2010) report that reducing energy consumption allows these cells to survive on ... ...

    Abstract Cells lacking a functional tuberous sclerosis complex (TSC) heterodimer are sensitized to glucose starvation-induced death. In this issue of Molecular Cell, Choo et al. (2010) report that reducing energy consumption allows these cells to survive on glutamine as an alternative energy source.
    Language English
    Publishing date 2010-05-28
    Publishing country United States
    Document type Comment ; Journal Article
    ZDB-ID 1415236-8
    ISSN 1097-4164 ; 1097-2765
    ISSN (online) 1097-4164
    ISSN 1097-2765
    DOI 10.1016/j.molcel.2010.05.008
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  4. Article ; Online: Glutaminolysis yields a metabolic by-product that stimulates autophagy.

    Eng, Christina H / Abraham, Robert T

    Autophagy

    2010  Volume 6, Issue 7, Page(s) 968–970

    Abstract: Autophagy is an intracellular degradative pathway that plays key roles in the homeostatic turnover of long-lived or damaged proteins and organelles, and in the survival of cells during starvation or other stressful conditions. We have uncovered an ... ...

    Abstract Autophagy is an intracellular degradative pathway that plays key roles in the homeostatic turnover of long-lived or damaged proteins and organelles, and in the survival of cells during starvation or other stressful conditions. We have uncovered an unexpected link between glutamine (Gln) metabolism and the regulation of autophagy. Our findings indicate that ammonia, generated from Gln deamination in mitochondria, functions as an autocrine- and/or paracrine-acting stimulator of autophagic flux.
    MeSH term(s) Ammonia/metabolism ; Autophagy/physiology ; Cell Line, Tumor ; Culture Media, Conditioned/chemistry ; Culture Media, Conditioned/metabolism ; Glutaminase/metabolism ; Glutamine/metabolism ; Humans ; Mitochondria/metabolism
    Chemical Substances Culture Media, Conditioned ; Glutamine (0RH81L854J) ; Ammonia (7664-41-7) ; Glutaminase (EC 3.5.1.2)
    Language English
    Publishing date 2010-10-20
    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 10.4161/auto.6.7.13082
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  5. Article ; Online: Mammalian target of rapamycin as a therapeutic target in oncology.

    Abraham, Robert T / Eng, Christina H

    Expert opinion on therapeutic targets

    2008  Volume 12, Issue 2, Page(s) 209–222

    Abstract: Background: The mammalian target of rapamycin (mTOR) has emerged as a validated therapeutic target in cancer and mTOR inhibitors alter tumor cell responses to mitogenic signals and microenvironmental stress.: Objectives: The aims of this review are ... ...

    Abstract Background: The mammalian target of rapamycin (mTOR) has emerged as a validated therapeutic target in cancer and mTOR inhibitors alter tumor cell responses to mitogenic signals and microenvironmental stress.
    Objectives: The aims of this review are to describe the mTOR signaling pathway and the rationale for the use of rapamycin analogs and other mTOR inhibitors for oncology indications.
    Methods: This review presents information from recent publications, as well as some more conjectural viewpoints stemming from the early clinical experience with mTOR inhibitors in cancer patients.
    Results/conclusions: A thorough understanding of the antitumor mechanisms of the existing mTOR inhibitors will drive the development of effective combination therapies to overcome tumor resistance to these agents. Furthermore, the development of second-generation inhibitors of this critical protein target may yield deeper and broader therapeutic activities in human cancers.
    MeSH term(s) Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Humans ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Protein Kinases/metabolism ; TOR Serine-Threonine Kinases
    Chemical Substances Antineoplastic Agents ; Protein Kinases (EC 2.7.-) ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1)
    Language English
    Publishing date 2008-01-02
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2055208-7
    ISSN 1744-7631 ; 1472-8222
    ISSN (online) 1744-7631
    ISSN 1472-8222
    DOI 10.1517/14728222.12.2.209
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    Zs.A 5244: Show issues Location:
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  6. Article: Anti-tumor immunity influences cancer cell reliance upon ATG7.

    Arensman, Michael D / Yang, Xiaoran S / Zhong, Wenyan / Bisulco, Stephanie / Upeslacis, Erik / Rosfjord, Edward C / Deng, Shibing / Abraham, Robert T / Eng, Christina H

    Oncoimmunology

    2020  Volume 9, Issue 1, Page(s) 1800162

    Abstract: Macroautophagy (autophagy) is an essential cellular catabolic process required for survival under conditions of starvation. The role of autophagy in cancer is complex, context-dependent and at times contradictory, as it has been shown to inhibit, promote ...

    Abstract Macroautophagy (autophagy) is an essential cellular catabolic process required for survival under conditions of starvation. The role of autophagy in cancer is complex, context-dependent and at times contradictory, as it has been shown to inhibit, promote or be dispensable for tumor progression. In this study, we evaluated the contribution of the immune system to the reliance of tumors on autophagy by depleting autophagy-related 7 (ATG7) in murine tumor cells and grafting into immunocompetent versus immunodeficient hosts. Although loss of ATG7 did not affect tumor growth in vitro or in immunodeficient mice, our studies revealed that cancer cell reliance on autophagy was influenced by anti-tumor immune responses, including those mediated by CD8
    MeSH term(s) Animals ; Autophagy ; Autophagy-Related Protein 7/genetics ; CD8-Positive T-Lymphocytes ; Humans ; Mice ; Neoplasms
    Chemical Substances Atg7 protein, mouse ; ATG7 protein, human (EC 6.2.1.45) ; Autophagy-Related Protein 7 (EC 6.2.1.45)
    Language English
    Publishing date 2020-08-23
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2645309-5
    ISSN 2162-402X ; 2162-4011
    ISSN (online) 2162-402X
    ISSN 2162-4011
    DOI 10.1080/2162402X.2020.1800162
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  7. Article ; Online: Cystine-glutamate antiporter xCT deficiency suppresses tumor growth while preserving antitumor immunity.

    Arensman, Michael D / Yang, Xiaoran S / Leahy, Danielle M / Toral-Barza, Lourdes / Mileski, Mary / Rosfjord, Edward C / Wang, Fang / Deng, Shibing / Myers, Jeremy S / Abraham, Robert T / Eng, Christina H

    Proceedings of the National Academy of Sciences of the United States of America

    2019  Volume 116, Issue 19, Page(s) 9533–9542

    Abstract: T cell-invigorating cancer immunotherapies have near-curative potential. However, their clinical benefit is currently limited, as only a fraction of patients respond, suggesting that these regimens may benefit from combination with tumor-targeting ... ...

    Abstract T cell-invigorating cancer immunotherapies have near-curative potential. However, their clinical benefit is currently limited, as only a fraction of patients respond, suggesting that these regimens may benefit from combination with tumor-targeting treatments. As oncogenic progression is accompanied by alterations in metabolic pathways, tumors often become heavily reliant on antioxidant machinery and may be susceptible to increases in oxidative stress. The cystine-glutamate antiporter xCT is frequently overexpressed in cancer and fuels the production of the antioxidant glutathione; thus, tumors prone to redox stress may be selectively vulnerable to xCT disruption. However, systemic inhibition of xCT may compromise antitumor immunity, as xCT is implicated in supporting antigen-induced T cell proliferation. Therefore, we utilized immune-competent murine tumor models to investigate whether cancer cell expression of xCT was required for tumor growth in vivo and if deletion of host xCT impacted antitumor immune responses. Deletion of xCT in tumor cells led to defective cystine uptake, accumulation of reactive oxygen species, and impaired tumor growth, supporting a cancer cell-autonomous role for xCT. In contrast, we observed that, although T cell proliferation in culture was exquisitely dependent on xCT expression, xCT was dispensable for T cell proliferation in vivo and for the generation of primary and memory immune responses to tumors. These findings prompted the combination of tumor cell xCT deletion with the immunotherapeutic agent anti-CTLA-4, which dramatically increased the frequency and durability of antitumor responses. Together, these results identify a metabolic vulnerability specific to tumors and demonstrate that xCT disruption can expand the efficacy of anticancer immunotherapies.
    MeSH term(s) Amino Acid Transport System y+/deficiency ; Amino Acid Transport System y+/immunology ; Animals ; Antigen-Presenting Cells/immunology ; Antigen-Presenting Cells/pathology ; Cell Line ; Cell Proliferation ; Gene Deletion ; Glutathione/genetics ; Glutathione/immunology ; Immunologic Memory ; Immunotherapy ; Mice ; Mice, Knockout ; Neoplasms, Experimental/genetics ; Neoplasms, Experimental/immunology ; Neoplasms, Experimental/pathology ; Neoplasms, Experimental/therapy ; T-Lymphocytes/immunology ; T-Lymphocytes/pathology
    Chemical Substances Amino Acid Transport System y+ ; Slc7a11 protein, mouse ; Glutathione (GAN16C9B8O)
    Language English
    Publishing date 2019-04-24
    Publishing country United States
    Document type Journal Article
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.1814932116
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  8. Article: The formin mDia regulates GSK3beta through novel PKCs to promote microtubule stabilization but not MTOC reorientation in migrating fibroblasts.

    Eng, Christina H / Huckaba, Thomas M / Gundersen, Gregg G

    Molecular biology of the cell

    2006  Volume 17, Issue 12, Page(s) 5004–5016

    Abstract: In migrating cells, external signals polarize the microtubule (MT) cytoskeleton by stimulating the formation of oriented, stabilized MTs and inducing the reorientation of the MT organizing center (MTOC). Glycogen synthase kinase 3beta (GSK3beta) has been ...

    Abstract In migrating cells, external signals polarize the microtubule (MT) cytoskeleton by stimulating the formation of oriented, stabilized MTs and inducing the reorientation of the MT organizing center (MTOC). Glycogen synthase kinase 3beta (GSK3beta) has been implicated in each of these processes, although whether it regulates both processes in a single system and how its activity is regulated are unclear. We examined these issues in wound-edge, serum-starved NIH 3T3 fibroblasts where MT stabilization and MTOC reorientation are triggered by lysophosphatidic acid (LPA), but are regulated independently by distinct Rho GTPase-signaling pathways. In the absence of other treatments, the GSK3beta inhibitors, LiCl or SB216763, induced the formation of stable MTs, but not MTOC reorientation, in starved fibroblasts. Overexpression of GSK3beta in starved fibroblasts inhibited LPA-induced stable MTs without inhibiting MTOC reorientation. Analysis of factors involved in stable MT formation (Rho, mDia, and EB1) showed that GSK3beta functioned upstream of EB1, but downstream of Rho-mDia. mDia was both necessary and sufficient for inducing stable MTs and for up-regulating GSK3beta phosphorylation on Ser9, an inhibitory site. mDia appears to regulate GSK3beta through novel class PKCs because PKC inhibitors and dominant negative constructs of novel PKC isoforms prevented phosphorylation of GSK3beta Ser9 and stable MT formation. Novel PKCs also interacted with mDia in vivo and in vitro. These results identify a new activity for the formin mDia in regulating GSK3beta through novel PKCs and implicate novel PKCs as new factors in the MT stabilization pathway.
    MeSH term(s) Anaphase-Promoting Complex-Cyclosome ; Animals ; COS Cells ; Carrier Proteins/metabolism ; Cell Movement/drug effects ; Cercopithecus aethiops ; Fibroblasts/cytology ; Fibroblasts/drug effects ; Glycogen Synthase Kinase 3/metabolism ; Glycogen Synthase Kinase 3 beta ; Isoenzymes/metabolism ; Lysophospholipids/pharmacology ; Mice ; Microtubule-Associated Proteins/metabolism ; Microtubule-Organizing Center/drug effects ; Microtubule-Organizing Center/metabolism ; Microtubules/drug effects ; Microtubules/metabolism ; NIH 3T3 Cells ; Phosphorylation/drug effects ; Protein Binding/drug effects ; Protein Kinase C/metabolism ; Ubiquitin-Protein Ligase Complexes/metabolism ; rho GTP-Binding Proteins/metabolism
    Chemical Substances Carrier Proteins ; Diap1 protein, mouse ; EB1 microtubule binding proteins ; Isoenzymes ; Lysophospholipids ; Microtubule-Associated Proteins ; Ubiquitin-Protein Ligase Complexes (EC 2.3.2.23) ; Anaphase-Promoting Complex-Cyclosome (EC 2.3.2.27) ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1) ; Gsk3b protein, mouse (EC 2.7.11.1) ; Protein Kinase C (EC 2.7.11.13) ; Glycogen Synthase Kinase 3 (EC 2.7.11.26) ; rho GTP-Binding Proteins (EC 3.6.5.2) ; lysophosphatidic acid (PG6M3969SG)
    Language English
    Publishing date 2006-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1098979-1
    ISSN 1939-4586 ; 1059-1524
    ISSN (online) 1939-4586
    ISSN 1059-1524
    DOI 10.1091/mbc.E05-10-0914
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  9. Article ; Online: Glutamine deprivation stimulates mTOR-JNK-dependent chemokine secretion.

    Shanware, Naval P / Bray, Kevin / Eng, Christina H / Wang, Fang / Follettie, Maximillian / Myers, Jeremy / Fantin, Valeria R / Abraham, Robert T

    Nature communications

    2014  Volume 5, Page(s) 4900

    Abstract: The non-essential amino acid, glutamine, exerts pleiotropic effects on cell metabolism, signalling and stress resistance. Here we demonstrate that short-term glutamine restriction triggers an endoplasmic reticulum (ER) stress response that leads to ... ...

    Abstract The non-essential amino acid, glutamine, exerts pleiotropic effects on cell metabolism, signalling and stress resistance. Here we demonstrate that short-term glutamine restriction triggers an endoplasmic reticulum (ER) stress response that leads to production of the pro-inflammatory chemokine, interleukin-8 (IL-8). Glutamine deprivation-induced ER stress triggers colocalization of autophagosomes, lysosomes and the Golgi into a subcellular structure whose integrity is essential for IL-8 secretion. The stimulatory effect of glutamine restriction on IL-8 production is attributable to depletion of tricarboxylic acid cycle intermediates. The protein kinase, mTOR, is also colocalized with the lysosomal membrane clusters induced by glutamine deprivation, and inhibition of mTORC1 activity abolishes both endomembrane reorganization and IL-8 secretion. Activated mTORC1 elicits IL8 gene expression via the activation of an IRE1-JNK signalling cascade. Treatment of cells with a glutaminase inhibitor phenocopies glutamine restriction, suggesting that these results will be relevant to the clinical development of glutamine metabolism inhibitors as anticancer agents.
    MeSH term(s) Cell Line, Tumor ; Citric Acid Cycle ; Endoplasmic Reticulum Stress ; Glutamine ; Humans ; Interleukin-8/metabolism ; Lysosomes/metabolism ; MAP Kinase Kinase 4/genetics ; MAP Kinase Kinase 4/metabolism ; Mechanistic Target of Rapamycin Complex 1 ; Multiprotein Complexes/genetics ; Multiprotein Complexes/metabolism ; TOR Serine-Threonine Kinases/genetics ; TOR Serine-Threonine Kinases/metabolism
    Chemical Substances Interleukin-8 ; Multiprotein Complexes ; Glutamine (0RH81L854J) ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; MAP Kinase Kinase 4 (EC 2.7.12.2)
    Language English
    Publishing date 2014-09-25
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/ncomms5900
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  10. Article ; Online: Ammonia derived from glutaminolysis is a diffusible regulator of autophagy.

    Eng, Christina H / Yu, Ker / Lucas, Judy / White, Eileen / Abraham, Robert T

    Science signaling

    2010  Volume 3, Issue 119, Page(s) ra31

    Abstract: Autophagy is a tightly regulated catabolic process that plays key roles in normal cellular homeostasis and survival during periods of extracellular nutrient limitation and stress. The environmental signals that regulate autophagic activity are only ... ...

    Abstract Autophagy is a tightly regulated catabolic process that plays key roles in normal cellular homeostasis and survival during periods of extracellular nutrient limitation and stress. The environmental signals that regulate autophagic activity are only partially understood. Here, we report a direct link between glutamine (Gln) metabolism and autophagic activity in both transformed and nontransformed human cells. Cells cultured for more than 2 days in Gln-containing medium showed increases in autophagy that were not attributable to nutrient depletion or to inhibition of mammalian target of rapamycin. Conditioned medium from these cells contained a volatile factor that triggered autophagy in secondary cell cultures. We identified this factor as ammonia derived from the deamination of Gln by glutaminolysis. Gln-dependent ammonia production supported basal autophagy and protected cells from tumor necrosis factor-alpha (TNF-alpha)-induced cell death. Thus, Gln metabolism not only fuels cell growth but also generates an autocrine- and paracrine-acting regulator of autophagic flux in proliferating cells.
    MeSH term(s) Ammonia/metabolism ; Autophagy ; Cells, Cultured ; Glutamine/metabolism ; Humans ; Hydrolysis
    Chemical Substances Glutamine (0RH81L854J) ; Ammonia (7664-41-7)
    Language English
    Publishing date 2010-04-27
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2417226-1
    ISSN 1937-9145 ; 1945-0877
    ISSN (online) 1937-9145
    ISSN 1945-0877
    DOI 10.1126/scisignal.2000911
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