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Article ; Online: Homeostatic Roles of STING in Cell Proliferation and Chromosomal Instability.

Gius, David / Zhu, Yueming

2019 Volume 79, Issue 7, Page(s) 1295–1296

Abstract: In this issue ... ...

Abstract	In this issue of
MeSH term(s)	Animals ; Cell Proliferation ; Cell Transformation, Neoplastic/genetics ; Chromosomal Instability ; Membrane Proteins/genetics ; Mice ; Neoplasms/genetics
Chemical Substances	Membrane Proteins
Language	English
Publishing date	2019-02-06
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-19-0212
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Article: Glycogen Phosphorylase: A Novel Biomarker in Doxorubicin-Induced Cardiac Injury.

Zhu, Yueming / Gius, David

Clinical cancer research : an official journal of the American Association for Cancer Research

2018 Volume 24, Issue 7, Page(s) 1516–1517

Abstract: Extracellular vesicles containing glycogen phosphorylase, brain/heart (PYGB) have been demonstrated as a sensitive biomarker for normal cardiac injuries for patients after chemotherapy. Oxidative stress was suggested to be the mechanism behind the ... ...

Abstract	Extracellular vesicles containing glycogen phosphorylase, brain/heart (PYGB) have been demonstrated as a sensitive biomarker for normal cardiac injuries for patients after chemotherapy. Oxidative stress was suggested to be the mechanism behind the chemotherapy-induced tissue damage and augmented with mitochondrial antioxidant could be an effective means of early intervention.
MeSH term(s)	Animals ; Biomarkers ; Doxorubicin ; Extracellular Vesicles ; Glycogen Phosphorylase ; Humans ; Mice ; Myocytes, Cardiac/drug effects
Chemical Substances	Biomarkers ; Doxorubicin (80168379AG) ; Glycogen Phosphorylase (EC 2.4.1.-)
Language	English
Publishing date	2018-01-22
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-17-3276
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Zs.A 4223: Show issues

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Article: Manganese Superoxide Dismutase Acetylation and Regulation of Protein Structure in Breast Cancer Biology and Therapy.

Ogle, Meredith M / Trevino, Rolando / Schell, Joseph / Varmazyad, Mahboubeh / Horikoshi, Nobuo / Gius, David

Antioxidants (Basel, Switzerland)

2022 Volume 11, Issue 4

Abstract: The loss and/or dysregulation of several cellular and mitochondrial antioxidants' expression or enzymatic activity, which leads to the aberrant physiological function of these proteins, has been shown to result in oxidative damage to cellular ... ...

Abstract	The loss and/or dysregulation of several cellular and mitochondrial antioxidants' expression or enzymatic activity, which leads to the aberrant physiological function of these proteins, has been shown to result in oxidative damage to cellular macromolecules. In this regard, it has been surmised that the disruption of mitochondrial networks responsible for maintaining normal metabolism is an established hallmark of cancer and a novel mechanism of therapy resistance. This altered metabolism leads to aberrant accumulation of reactive oxygen species (ROS), which, under specific physiological conditions, leads to a potential tumor-permissive cellular environment. In this regard, it is becoming increasingly clear that the loss or disruption of mitochondrial oxidant scavenging enzymes may be, in specific tumors, either an early event in transformation or exhibit tumor-promoting properties. One example of such an antioxidant enzyme is manganese superoxide dismutase (MnSOD, also referred to as SOD2), which detoxifies superoxide, a ROS that has been shown, when its normal physiological levels are disrupted, to lead to oncogenicity and therapy resistance. Here, we will also discuss how the acetylation of MnSOD leads to a change in detoxification function that leads to a cellular environment permissive for the development of lineage plasticity-like properties that may be one mechanism leading to tumorigenic and therapy-resistant phenotypes.
Language	English
Publishing date	2022-03-25
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox11040635
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Article ; Online: Coordinated Specialty Care Discharge, Transition, and Step-Down Policies, Practices, and Concerns: Staff and Client Perspectives.

Jones, Nev / Gius, Becky / Daley, Tamara / George, Preethy / Rosenblatt, Abram / Shern, David

Psychiatric services (Washington, D.C.)

2020 Volume 71, Issue 5, Page(s) 487–497

Abstract: Objective: In recent years, optimizing the process of transition and discharge from coordinated specialty care (CSC), a program that provides early intervention in psychosis, has emerged as an important focus area for program administrators, clinicians, ...

Abstract	Objective: In recent years, optimizing the process of transition and discharge from coordinated specialty care (CSC), a program that provides early intervention in psychosis, has emerged as an important focus area for program administrators, clinicians, and policy makers. To explore existing CSC policies and practices and to understand frontline provider and client views on discharge, the authors conducted a comprehensive analysis of staff and client interview data from the Mental Health Block Grant 10% Set-Aside Study. Methods: Data from 66 interviews with groups of CSC providers and administrators representing 36 sites and 22 states were analyzed, as well as data from interviews with 82 CSC clients at 34 sites. Transcripts were coded by using systematic content analyses. Results: Analyses of data from providers and administrators showed the heterogeneity of CSC program practices and strategies regarding discharge and highlighted a range of concerns related to postdischarge service accessibility and quality. Analysis of data from client interviews reflected the heterogeneity of transition challenges that clients confront. A significant number of participants reported concerns about their readiness for discharge. Conclusions: CSC discharge policies and practices vary across CSC programs and states. Frequent clinician and client concerns about optimal program length, transition, and postdischarge services highlight the importance of sustained policy and research efforts to develop evidence-informed practice guidelines and possible modifications to the time-limited CSC model that currently dominates the field.
MeSH term(s)	Adolescent ; Adult ; Aftercare ; Attitude of Health Personnel ; Female ; Health Policy ; Humans ; Interviews as Topic ; Longitudinal Studies ; Male ; Mental Health Services ; Patient Acceptance of Health Care ; Patient Discharge ; Program Development ; Psychotic Disorders/therapy ; Qualitative Research ; United States ; Young Adult
Language	English
Publishing date	2020-03-19
Publishing country	United States
Document type	Journal Article ; Multicenter Study ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	1220173-x
ISSN	1557-9700 ; 1075-2730
ISSN (online)	1557-9700
ISSN	1075-2730
DOI	10.1176/appi.ps.201900514
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Zs.A 416: Show issues

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Article ; Online: MnSOD Lysine 68 acetylation leads to cisplatin and doxorubicin resistance due to aberrant mitochondrial metabolism.

Gao, Yucheng / Zhu, Yueming / Tran, Elizabeth L / Tokars, Valerie / Dean, Angela E / Quan, Songhua / Gius, David

International journal of biological sciences

2021 Volume 17, Issue 5, Page(s) 1203–1216

Abstract: Manganese superoxide dismutase (MnSOD) acetylation (Ac) has been shown to be a key post-translational modification important in the regulation of detoxification activity in various disease models. We have previously demonstrated that MnSOD lysine-68 (K68) ...

Abstract	Manganese superoxide dismutase (MnSOD) acetylation (Ac) has been shown to be a key post-translational modification important in the regulation of detoxification activity in various disease models. We have previously demonstrated that MnSOD lysine-68 (K68) acetylation (K68-Ac) leads to a change in function from a superoxide-scavenging homotetramer to a peroxidase-directed monomer. Here, we found that estrogen receptor positive (ER+) breast cancer cell lines (MCF7 and T47D), selected for continuous growth in cisplatin (CDDP) and doxorubicin (DXR), exhibited an increase in MnSOD-K68-Ac. In addition, MnSOD-K68-Ac, as modeled by the expression of a validated acetylation mimic mutant gene (
MeSH term(s)	Acetylation ; Animals ; Antineoplastic Agents/pharmacology ; Breast Neoplasms/drug therapy ; Breast Neoplasms/metabolism ; Carcinogenesis/drug effects ; Carcinogenesis/metabolism ; Cell Line, Tumor ; Cisplatin/pharmacology ; Doxorubicin/pharmacology ; Drug Resistance, Neoplasm ; Free Radical Scavengers/metabolism ; Humans ; Inactivation, Metabolic ; MCF-7 Cells ; Mice ; Mitochondria/drug effects ; Mitochondria/metabolism ; Protein Processing, Post-Translational ; Sirtuins/metabolism ; Superoxide Dismutase/metabolism
Chemical Substances	Antineoplastic Agents ; Free Radical Scavengers ; Doxorubicin (80168379AG) ; Superoxide Dismutase (EC 1.15.1.1) ; Sirtuins (EC 3.5.1.-) ; Cisplatin (Q20Q21Q62J)
Language	English
Publishing date	2021-03-19
Publishing country	Australia
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2179208-2
ISSN	1449-2288 ; 1449-2288
ISSN (online)	1449-2288
ISSN	1449-2288
DOI	10.7150/ijbs.51184
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Article: Redox-sensitive signaling factors and antioxidants: how tumor cells respond to ionizing radiation.

Gius, David

The Journal of nutrition

2003 Volume 134, Issue 11, Page(s) 3213S–3214S

MeSH term(s)	Antioxidants/pharmacology ; Cysteine/chemistry ; Cysteine/physiology ; DNA Damage ; Free Radicals ; Humans ; Hydrogen Peroxide/pharmacology ; Neoplasms/radiotherapy ; Oxidation-Reduction ; Oxidative Stress ; Radiation, Ionizing ; Signal Transduction ; Thioredoxin-Disulfide Reductase/metabolism ; Thioredoxins/chemistry ; Thioredoxins/metabolism
Chemical Substances	Antioxidants ; Free Radicals ; Thioredoxins (52500-60-4) ; Hydrogen Peroxide (BBX060AN9V) ; Thioredoxin-Disulfide Reductase (EC 1.8.1.9) ; Cysteine (K848JZ4886)
Language	English
Publishing date	2003-05-14
Publishing country	United States
Document type	Journal Article
ZDB-ID	218373-0
ISSN	1541-6100 ; 0022-3166
ISSN (online)	1541-6100
ISSN	0022-3166
DOI	10.1093/jn/134.11.3213S
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Article ; Online: An engineered chimeric toxin that cleaves activated mutant and wild-type RAS inhibits tumor growth.

Vidimar, Vania / Beilhartz, Greg L / Park, Minyoung / Biancucci, Marco / Kieffer, Matthew B / Gius, David R / Melnyk, Roman A / Satchell, Karla J F

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

2020 Volume 117, Issue 29, Page(s) 16938–16948

Abstract: Despite nearly four decades of effort, broad inhibition of oncogenic RAS using small-molecule approaches has proven to be a major challenge. Here we describe the development of a pan-RAS biologic inhibitor composed of the RAS-RAP1-specific endopeptidase ... ...

Abstract	Despite nearly four decades of effort, broad inhibition of oncogenic RAS using small-molecule approaches has proven to be a major challenge. Here we describe the development of a pan-RAS biologic inhibitor composed of the RAS-RAP1-specific endopeptidase fused to the protein delivery machinery of diphtheria toxin. We show that this engineered chimeric toxin irreversibly cleaves and inactivates intracellular RAS at low picomolar concentrations terminating downstream signaling in receptor-bearing cells. Furthermore, we demonstrate in vivo target engagement and reduction of tumor burden in three mouse xenograft models driven by either wild-type or mutant
MeSH term(s)	Animals ; Antineoplastic Agents/therapeutic use ; Cells, Cultured ; Diphtheria Toxin/chemistry ; Diphtheria Toxin/genetics ; Diphtheria Toxin/metabolism ; Endopeptidases/chemistry ; Endopeptidases/genetics ; Endopeptidases/metabolism ; Female ; HCT116 Cells ; Humans ; Male ; Mice ; Mice, Nude ; Mutation ; Neoplasms, Experimental/drug therapy ; Protein Sorting Signals ; Proteolysis ; Recombinant Proteins/therapeutic use ; rap1 GTP-Binding Proteins/metabolism ; ras Proteins/genetics ; ras Proteins/metabolism
Chemical Substances	Antineoplastic Agents ; Diphtheria Toxin ; Protein Sorting Signals ; Recombinant Proteins ; Endopeptidases (EC 3.4.-) ; Rap1 protein, mouse (EC 3.6.5.2) ; rap1 GTP-Binding Proteins (EC 3.6.5.2) ; ras Proteins (EC 3.6.5.2)
Language	English
Publishing date	2020-07-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2000312117
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Zs.A 1148: Show issues

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Article ; Online: Regulation of KLF4 by posttranslational modification circuitry in endocrine resistance.

Zhou, Zhuan / Song, Xinxin / Chi, Junlong Jack / Gius, David R / Huang, Yi / Cristofanilli, Massimo / Wan, Yong

Cellular signalling

2020 Volume 70, Page(s) 109574

Abstract: KLF4 plays an important role in orchestrating a variety of cellular events, including cell-fate decision, genome stability and apoptosis. Its deregulation is correlated with human diseases such as breast cancer and gastrointestinal cancer. Results from ... ...

Abstract	KLF4 plays an important role in orchestrating a variety of cellular events, including cell-fate decision, genome stability and apoptosis. Its deregulation is correlated with human diseases such as breast cancer and gastrointestinal cancer. Results from recent biochemical studies have revealed that KLF4 is tightly regulated by posttranslational modifications. Here we report a new finding that KLF4 orchestrates estrogen receptor signaling and facilitates endocrine resistance. We also uncovered the underlying mechanism that alteration of KLF4 by posttranslational modifications such as phosphorylation and ubiquitylation changes tumor cell response to endocrine therapy drugs. IHC analyses using based on human breast cancer specimens showed the accumulation of KLF4 protein in ER-positive breast cancer tissues. Elevated KLF4 expression significantly correlated with prognosis and endocrine resistance. Our drug screening for suppressing KLF4 protein expression led to identification of Src kinase to be a critical player in modulating KLF4-mediated tamoxifen resistance. Depletion of VHL (von Hippel-Lindau tumor suppressor), a ubiquitin E3 ligase for KLF4, reduces tumor cell sensitivity to tamoxifen. We demonstrated phosphorylation of VHL by Src enhances proteolysis of VHL that in turn leads to upregulation of KLF4 and increases endocrine resistance. Suppression of Src-VHL-KLF4 cascade by Src inhibitor or enhancement of VHL-KLF4 ubiquitination by TAT-KLF4 (371-420AAa) peptides re-sensitizes tamoxifen-resistant breast cancer cells to tamoxifen treatment. Taken together, our findings demonstrate a novel role for KLF4 in modulating endocrine resistance via the Src-VHL-KLF4 axis.
MeSH term(s)	Breast Neoplasms/metabolism ; Drug Resistance, Neoplasm ; Gene Expression Regulation, Neoplastic ; HEK293 Cells ; Humans ; Kruppel-Like Factor 4 ; Kruppel-Like Transcription Factors/physiology ; MCF-7 Cells ; Von Hippel-Lindau Tumor Suppressor Protein/metabolism
Chemical Substances	KLF4 protein, human ; Kruppel-Like Factor 4 ; Kruppel-Like Transcription Factors ; Von Hippel-Lindau Tumor Suppressor Protein (EC 2.3.2.27) ; VHL protein, human (EC 6.3.2.-)
Language	English
Publishing date	2020-02-19
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1002702-6
ISSN	1873-3913 ; 0898-6568
ISSN (online)	1873-3913
ISSN	0898-6568
DOI	10.1016/j.cellsig.2020.109574
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Zs.A 2579: Show issues

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Article ; Online: SIRT3 Overexpression Ameliorates Asbestos-Induced Pulmonary Fibrosis, mt-DNA Damage, and Lung Fibrogenic Monocyte Recruitment.

Cheresh, Paul / Kim, Seok-Jo / Jablonski, Renea / Watanabe, Satoshi / Lu, Ziyan / Chi, Monica / Helmin, Kathryn A / Gius, David / Budinger, G R Scott / Kamp, David W

International journal of molecular sciences

2021 Volume 22, Issue 13

Abstract: Alveolar epithelial cell (AEC) mitochondrial (mt) DNA damage and fibrotic monocyte-derived alveolar macrophages (Mo-AMs) are implicated in the pathobiology of pulmonary fibrosis. We showed that sirtuin 3 (SIRT3), a mitochondrial protein regulating cell ... ...

Abstract	Alveolar epithelial cell (AEC) mitochondrial (mt) DNA damage and fibrotic monocyte-derived alveolar macrophages (Mo-AMs) are implicated in the pathobiology of pulmonary fibrosis. We showed that sirtuin 3 (SIRT3), a mitochondrial protein regulating cell fate and aging, is deficient in the AECs of idiopathic pulmonary fibrosis (IPF) patients and that asbestos- and bleomycin-induced lung fibrosis is augmented in Sirt3 knockout (
MeSH term(s)	Animals ; Asbestos/adverse effects ; Biomarkers ; DNA Damage ; DNA, Mitochondrial ; Disease Models, Animal ; Gene Expression ; Humans ; Idiopathic Pulmonary Fibrosis/etiology ; Idiopathic Pulmonary Fibrosis/metabolism ; Idiopathic Pulmonary Fibrosis/pathology ; Immunohistochemistry ; Mice ; Mice, Transgenic ; Mitochondria/genetics ; Mitochondria/metabolism ; Monocytes/immunology ; Monocytes/metabolism ; Monocytes/pathology ; Oxidative Stress ; Sirtuin 3/genetics ; Sirtuin 3/metabolism
Chemical Substances	Biomarkers ; DNA, Mitochondrial ; Asbestos (1332-21-4) ; SIRT3 protein, human (EC 3.5.1.-) ; Sirtuin 3 (EC 3.5.1.-)
Language	English
Publishing date	2021-06-25
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22136856
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Article ; Online: Emerging evidence for targeting mitochondrial metabolic dysfunction in cancer therapy.

Zhu, Yueming / Dean, Angela Elizabeth / Horikoshi, Nobuo / Heer, Collin / Spitz, Douglas R / Gius, David

The Journal of clinical investigation

2018 Volume 128, Issue 9, Page(s) 3682–3691

Abstract: Mammalian cells use a complex network of redox-dependent processes necessary to maintain cellular integrity during oxidative metabolism, as well as to protect against and/or adapt to stress. The disruption of these redox-dependent processes, including ... ...

Abstract	Mammalian cells use a complex network of redox-dependent processes necessary to maintain cellular integrity during oxidative metabolism, as well as to protect against and/or adapt to stress. The disruption of these redox-dependent processes, including those in the mitochondria, creates a cellular environment permissive for progression to a malignant phenotype and the development of resistance to commonly used anticancer agents. An extension of this paradigm is that when these mitochondrial functions are altered by the events leading to transformation and ensuing downstream metabolic processes, they can be used as molecular biomarkers or targets in the development of new therapeutic interventions to selectively kill and/or sensitize cancer versus normal cells. In this Review we propose that mitochondrial oxidative metabolism is altered in tumor cells, and the central theme of this dysregulation is electron transport chain activity, folate metabolism, NADH/NADPH metabolism, thiol-mediated detoxification pathways, and redox-active metal ion metabolism. It is proposed that specific subgroups of human malignancies display distinct mitochondrial transformative and/or tumor signatures that may benefit from agents that target these pathways.
MeSH term(s)	Animals ; Female ; Gene Expression ; Humans ; Male ; Mitochondria/metabolism ; Mitochondrial Proteins/metabolism ; Models, Biological ; NAD/metabolism ; NADP/metabolism ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/therapy ; Oxidation-Reduction ; Oxidative Stress ; Protein Transport ; Signal Transduction ; Sirtuins/metabolism
Chemical Substances	Mitochondrial Proteins ; NAD (0U46U6E8UK) ; NADP (53-59-8) ; Sirtuins (EC 3.5.1.-)
Language	English
Publishing date	2018-08-31
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI120844
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