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Article ; Online: miR-217 Regulates Normal and Tumor Cell Fate Following Induction of Endoplasmic Reticulum Stress.

Dey, Neekkan / Koumenis, Costas / Ruggero, Davide / Fuchs, Serge Y / Diehl, J Alan

2024 Volume 22, Issue 4, Page(s) 360–372

Abstract: Rapidly proliferating cancer cells require a microenvironment where essential metabolic nutrients like glucose, oxygen, and growth factors become scarce as the tumor volume surpasses the established vascular capacity of the tissue. Limits in nutrient ... ...

Abstract	Rapidly proliferating cancer cells require a microenvironment where essential metabolic nutrients like glucose, oxygen, and growth factors become scarce as the tumor volume surpasses the established vascular capacity of the tissue. Limits in nutrient availability typically trigger growth arrest and/or apoptosis to prevent cellular expansion. However, tumor cells frequently co-opt cellular survival pathways thereby favoring cell survival under this environmental stress. The unfolded protein response (UPR) pathway is typically engaged by tumor cells to favor adaptation to stress. PERK, an endoplasmic reticulum (ER) protein kinase and UPR effector is activated in tumor cells and contributes tumor cell adaptation by limiting protein translation and balancing redox stress. PERK also induces miRNAs that contribute to tumor adaptation. miR-211 and miR-216b were previously identified as PERK-ATF4-regulated miRNAs that regulate cell survival. We have identified another PERK-responsive miRNA, miR-217, with increased expression under prolonged ER stress. Key targets of miR-217 are identified as TRPM1, the host gene for miR-211 and EZH2. Evidence is provided that miR-217 expression is essential for the rapid loss of miR-211 in prolonged ER stress and provides a functional link for determining whether cells adapt to stress or commit to apoptosis. Implications: PERK-dependent induction of miR-217 limits accumulation and function of the prosurvival miRNA, miR-211, to establish cell fate and promote cell commitment to apoptosis.
MeSH term(s)	Humans ; eIF-2 Kinase/genetics ; eIF-2 Kinase/metabolism ; Endoplasmic Reticulum Stress/genetics ; Unfolded Protein Response ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Apoptosis/physiology ; Neoplasms/genetics ; Tumor Microenvironment ; TRPM Cation Channels/genetics
Chemical Substances	eIF-2 Kinase (EC 2.7.11.1) ; MicroRNAs ; TRPM1 protein, human ; TRPM Cation Channels ; MIRN217 microRNA, human
Language	English
Publishing date	2024-01-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	2098788-2
ISSN	1557-3125 ; 1541-7786
ISSN (online)	1557-3125
ISSN	1541-7786
DOI	10.1158/1541-7786.MCR-23-0676
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Zs.A 5744: Show issues

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Article ; Online: Hope and fear for interferon: the receptor-centric outlook on the future of interferon therapy.

Fuchs, Serge Y

Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research

2013 Volume 33, Issue 4, Page(s) 211–225

Abstract: After several decades of intense clinical research, the great promise of Type I interferons (IFN1) as the anticancer wonder drugs that could cure or, at the very least, curb the progression of various oncological diseases has regrettably failed to ... ...

Abstract	After several decades of intense clinical research, the great promise of Type I interferons (IFN1) as the anticancer wonder drugs that could cure or, at the very least, curb the progression of various oncological diseases has regrettably failed to deliver. Severe side effects and low efficacy of IFN1-based pharmaceutics greatly limited use of these drugs and further reduced the enthusiasm of clinical oncologists for future optimization of IFN1-based therapeutic modalities. Incredibly, extensive clinical studies to assess the efficacy of IFN1 alone or in combination with other anticancer drugs have not been paralleled by an equal scope in defining the determinants that confer cell sensitivity or refractoriness to IFN1. Given that all effects of IFN1 on malignant and benign cells alike are mediated by its receptor, the mechanisms regulating these receptor cell surface levels should play a paramount role in shaping the magnitude and duration of IFN1-elicited effects. These mechanisms and their role in controlling IFN1 responses, as well as an ability of a growing tumor to commandeer these events, are the focus of our review. We postulate that activation of numerous signaling pathways leading to elimination of IFN1 receptor occurs in cancer cells and benign cells that contribute to tumor tissue. We further hypothesize that activation of these eliminative pathways enables the escape from IFN1-driven suppression of tumorigenesis and elicits the primary refractoriness of tumor to the pharmaceutical IFN1.
MeSH term(s)	Drug Resistance, Neoplasm ; Humans ; Interferon Type I/adverse effects ; Interferon Type I/therapeutic use ; Neoplasms/drug therapy ; Receptor, Interferon alpha-beta/metabolism ; Receptors, Interferon/metabolism ; Signal Transduction
Chemical Substances	IFNAR1 protein, human ; Interferon Type I ; Receptors, Interferon ; Receptor, Interferon alpha-beta (156986-95-7)
Language	English
Publishing date	2013-04-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1226675-9
ISSN	1557-7465 ; 1079-9907
ISSN (online)	1557-7465
ISSN	1079-9907
DOI	10.1089/jir.2012.0117
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Zs.A 1748: Show issues

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Article ; Online: Anti-metastatic functions of type 1 interferons: Foundation for the adjuvant therapy of cancer.

Ortiz, Angélica / Fuchs, Serge Y

Cytokine

2017 Volume 89, Page(s) 4–11

Abstract: The anti-tumorigenic effects that type 1 interferons (IFN1) elicited in the in vitro studies prompted consideration of IFN1 as a potent candidate for clinical treatment. Though not all patients responded to IFN1, clinical trials have shown that patients ... ...

Abstract	The anti-tumorigenic effects that type 1 interferons (IFN1) elicited in the in vitro studies prompted consideration of IFN1 as a potent candidate for clinical treatment. Though not all patients responded to IFN1, clinical trials have shown that patients with high risk melanoma, a highly refractory solid malignancy, benefit greatly from intermediate IFN1 treatment in regards to relapse-free and distant-metastasis-free survival. The mechanisms by which IFN1 treatment at early stages of disease suppress tumor recurrence or metastatic incidence are not fully understood. Intracellular IFN1 signaling is known to affect cell differentiation, proliferation, and apoptosis. Moreover, recent studies have revealed specific IFN1-regulated genes that may contribute to IFN1-mediated suppression of cancer progression and metastasis. In concert, expression of these different IFN1 stimulated genes may impede numerous mechanisms that mediate metastatic process. Though, IFN1 treatment is still utilized as part of standard care for metastatic melanoma (alone or in combination with other therapies), cancers find the ways to develop insensitivity to IFN1 treatment allowing for unconstrained disease progression. To determine how and when IFN1 treatment would be most efficacious during disease progression, we must understand how IFN1 signaling affects different metastasis steps. Here, we specifically focus on the anti-metastatic role of endogenous IFN1 and parameters that may help to use pharmaceutical IFN1 in the adjuvant treatment to prevent cancer recurrence and metastatic disease.
Language	English
Publishing date	2017-01
Publishing country	England
Document type	Review ; Journal Article
ZDB-ID	1018055-2
ISSN	1096-0023 ; 1043-4666
ISSN (online)	1096-0023
ISSN	1043-4666
DOI	10.1016/j.cyto.2016.01.010
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Zs.A 2840: Show issues

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Article ; Online: Ubiquitination-mediated regulation of interferon responses.

Fuchs, Serge Y

Growth factors (Chur, Switzerland)

2012 Volume 30, Issue 3, Page(s) 141–148

Abstract: Interferon cytokine family members shape the immune response to protect the host from both pathologic infections and tumorigenesis. To mediate their physiologic function, interferons evoke a robust and complex signal transduction pathway that leads to ... ...

Abstract	Interferon cytokine family members shape the immune response to protect the host from both pathologic infections and tumorigenesis. To mediate their physiologic function, interferons evoke a robust and complex signal transduction pathway that leads to the induction of interferon-stimulated genes with both proinflammatory and antiviral functions. Numerous mechanisms exist to tightly regulate the extent and duration of these cellular responses. Among such mechanisms, the post-translational conjugation of ubiquitin polypeptides to protein mediators of interferon signaling has emerged as a crucially important mode of control. In this mini-review, we highlight recent advances in our understanding of these ubiquitin-mediated mechanisms, their exploitation by invading viruses, and their possible utilization for medical intervention.
MeSH term(s)	Amino Acid Sequence ; Animals ; Gene Expression Regulation ; Humans ; Interferons/immunology ; Interferons/metabolism ; Molecular Sequence Data ; Signal Transduction/physiology ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/metabolism ; Ubiquitination ; Viruses/immunology ; Viruses/metabolism
Chemical Substances	Ubiquitin ; Interferons (9008-11-1) ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
Keywords	covid19
Language	English
Publishing date	2012-03-07
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1035755-5
ISSN	1029-2292 ; 0897-7194
ISSN (online)	1029-2292
ISSN	0897-7194
DOI	10.3109/08977194.2012.669382
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Zs.A 2612: Show issues

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Article ; Online: A DUB for MITF: no myth, some dubiety.

Fuchs, Serge Y

Pigment cell & melanoma research

2011 Volume 24, Issue 5, Page(s) 877–878

MeSH term(s)	Endopeptidases/metabolism ; Humans ; Melanoma/metabolism ; Microphthalmia-Associated Transcription Factor/chemistry
Chemical Substances	Microphthalmia-Associated Transcription Factor ; Endopeptidases (EC 3.4.-)
Language	English
Publishing date	2011-11-10
Publishing country	England
Document type	News ; Comment
ZDB-ID	2409570-9
ISSN	1755-148X ; 1600-0749 ; 0893-5785 ; 1755-1471
ISSN (online)	1755-148X ; 1600-0749
ISSN	0893-5785 ; 1755-1471
DOI	10.1111/j.1755-148x.2011.00900.x
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Zs.A 2444: Show issues

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Article ; Online: SCF ubiquitin E3 ligase regulates DNA double-strand breaks in early meiotic recombination.

Guan, Yongjuan / Lin, Huijuan / Leu, N Adrian / Ruthel, Gordon / Fuchs, Serge Y / Busino, Luca / Luo, Mengcheng / Wang, P Jeremy

Nucleic acids research

2022 Volume 50, Issue 9, Page(s) 5129–5144

Abstract: Homeostasis of meiotic DNA double strand breaks (DSB) is critical for germline genome integrity and homologous recombination. Here we demonstrate an essential role for SKP1, a constitutive subunit of the SCF (SKP1-Cullin-F-box) ubiquitin E3 ligase, in ... ...

Abstract	Homeostasis of meiotic DNA double strand breaks (DSB) is critical for germline genome integrity and homologous recombination. Here we demonstrate an essential role for SKP1, a constitutive subunit of the SCF (SKP1-Cullin-F-box) ubiquitin E3 ligase, in early meiotic processes. SKP1 restrains accumulation of HORMAD1 and the pre-DSB complex (IHO1-REC114-MEI4) on the chromosome axis in meiotic germ cells. Loss of SKP1 prior to meiosis leads to aberrant localization of DSB repair proteins and a failure in synapsis initiation in meiosis of both males and females. Furthermore, SKP1 is crucial for sister chromatid cohesion during the pre-meiotic S-phase. Mechanistically, FBXO47, a meiosis-specific F-box protein, interacts with SKP1 and HORMAD1 and targets HORMAD1 for polyubiquitination and degradation in HEK293T cells. Our results support a model wherein the SCF ubiquitin E3 ligase prevents hyperactive DSB formation through proteasome-mediated degradation of HORMAD1 and subsequent modulation of the pre-DSB complex during meiosis.
MeSH term(s)	Cell Cycle Proteins/metabolism ; DNA ; DNA Breaks, Double-Stranded ; Female ; HEK293 Cells ; Homologous Recombination ; Humans ; Male ; Meiosis/genetics ; SKP Cullin F-Box Protein Ligases/genetics ; Transcription Factors/genetics ; Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/metabolism ; Ubiquitins/genetics
Chemical Substances	Cell Cycle Proteins ; FBXO47 protein, human ; Transcription Factors ; Ubiquitins ; DNA (9007-49-2) ; SKP Cullin F-Box Protein Ligases (EC 2.3.2.27) ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
Language	English
Publishing date	2022-05-01
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gkac304
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Zs.A 1067: Show issues

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Article ; Online: An immunosuppressive vascular niche drives macrophage polarization and immunotherapy resistance in glioblastoma.

Yang, Fan / Akhtar, Md Naushad / Zhang, Duo / El-Mayta, Rakan / Shin, Junyoung / Dorsey, Jay F / Zhang, Lin / Xu, Xiaowei / Guo, Wei / Bagley, Stephen J / Fuchs, Serge Y / Koumenis, Constantinos / Lathia, Justin D / Mitchell, Michael J / Gong, Yanqing / Fan, Yi

Science advances

2024 Volume 10, Issue 9, Page(s) eadj4678

Abstract: Cancer immunity is subjected to spatiotemporal regulation by leukocyte interaction with neoplastic and stromal cells, contributing to immune evasion and immunotherapy resistance. Here, we identify a distinct mesenchymal-like population of endothelial ... ...

Abstract	Cancer immunity is subjected to spatiotemporal regulation by leukocyte interaction with neoplastic and stromal cells, contributing to immune evasion and immunotherapy resistance. Here, we identify a distinct mesenchymal-like population of endothelial cells (ECs) that form an immunosuppressive vascular niche in glioblastoma (GBM). We reveal a spatially restricted, Twist1/SATB1-mediated sequential transcriptional activation mechanism, through which tumor ECs produce osteopontin to promote immunosuppressive macrophage (Mφ) phenotypes. Genetic or pharmacological ablation of Twist1 reverses Mφ-mediated immunosuppression and enhances T cell infiltration and activation, leading to reduced GBM growth and extended mouse survival, and sensitizing tumor to chimeric antigen receptor T immunotherapy. Thus, these findings uncover a spatially restricted mechanism controlling tumor immunity and suggest that targeting endothelial Twist1 may offer attractive opportunities for optimizing cancer immunotherapy.
MeSH term(s)	Animals ; Mice ; Glioblastoma/genetics ; Endothelial Cells/pathology ; Cell Line, Tumor ; Macrophages ; Immunosuppression Therapy ; Brain Neoplasms/genetics
Language	English
Publishing date	2024-02-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.adj4678
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Article ; Online: ATF3 and CH25H regulate effector trogocytosis and anti-tumor activities of endogenous and immunotherapeutic cytotoxic T lymphocytes.

Lu, Zhen / McBrearty, Noreen / Chen, Jinyun / Tomar, Vivek S / Zhang, Hongru / De Rosa, Gianluca / Tan, Aiwen / Weljie, Aalim M / Beiting, Daniel P / Miao, Zhen / George, Subin S / Berger, Allison / Saggu, Gurpanna / Diehl, J Alan / Koumenis, Constantinos / Fuchs, Serge Y

Cell metabolism

2024 Volume 36, Issue 5, Page(s) 1164–1167

Language	English
Publishing date	2024-04-11
Publishing country	United States
Document type	Published Erratum
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2024.04.002
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Zs.A 6169: Show issues

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Article ; Online: Tumor-Derived Small Extracellular Vesicles Inhibit the Efficacy of CAR T Cells against Solid Tumors.

Zhong, Wenqun / Xiao, Zebin / Qin, Zhiyuan / Yang, Jingbo / Wen, Yi / Yu, Ziyan / Li, Yumei / Sheppard, Neil C / Fuchs, Serge Y / Xu, Xiaowei / Herlyn, Meenhard / June, Carl H / Puré, Ellen / Guo, Wei

Cancer research

2023 Volume 83, Issue 16, Page(s) 2790–2806

Abstract: Chimeric antigen receptor (CAR) T-cell therapy has shown remarkable success in the treatment of hematologic malignancies. Unfortunately, it has limited efficacy against solid tumors, even when the targeted antigens are well expressed. A better ... ...

Abstract	Chimeric antigen receptor (CAR) T-cell therapy has shown remarkable success in the treatment of hematologic malignancies. Unfortunately, it has limited efficacy against solid tumors, even when the targeted antigens are well expressed. A better understanding of the underlying mechanisms of CAR T-cell therapy resistance in solid tumors is necessary to develop strategies to improve efficacy. Here we report that solid tumors release small extracellular vesicles (sEV) that carry both targeted tumor antigens and the immune checkpoint protein PD-L1. These sEVs acted as cell-free functional units to preferentially interact with cognate CAR T cells and efficiently inhibited their proliferation, migration, and function. In syngeneic mouse tumor models, blocking tumor sEV secretion not only boosted the infiltration and antitumor activity of CAR T cells but also improved endogenous antitumor immunity. These results suggest that solid tumors use sEVs as an active defense mechanism to resist CAR T cells and implicate tumor sEVs as a potential therapeutic target to optimize CAR T-cell therapy against solid tumors. Significance: Small extracellular vesicles secreted by solid tumors inhibit CAR T cells, which provide a molecular explanation for CAR T-cell resistance and suggests that strategies targeting exosome secretion may enhance CAR T-cell efficacy. See related commentary by Ortiz-Espinosa and Srivastava, p. 2637.
MeSH term(s)	Animals ; Mice ; Cell Line, Tumor ; Neoplasms/metabolism ; T-Lymphocytes ; Immunotherapy, Adoptive/methods ; Antigens, Neoplasm ; Disease Models, Animal ; Extracellular Vesicles/metabolism ; Receptors, Antigen, T-Cell
Chemical Substances	Antigens, Neoplasm ; Receptors, Antigen, T-Cell
Language	English
Publishing date	2023-04-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-22-2220
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Uh III Zs.135/5: Show issues

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Article ; Online: Age-Dependent Effects of Type I and Type III IFNs in the Pathogenesis of

Ardanuy, Jeremy / Scanlon, Karen / Skerry, Ciaran / Fuchs, Serge Y / Carbonetti, Nicholas H

Journal of immunology (Baltimore, Md. : 1950)

2020 Volume 204, Issue 8, Page(s) 2192–2202

Abstract: Type I and III IFNs play diverse roles in bacterial infections, being protective for some but deleterious for others. Using RNA-sequencing transcriptomics we investigated lung gene expression responses ... ...

Abstract	Type I and III IFNs play diverse roles in bacterial infections, being protective for some but deleterious for others. Using RNA-sequencing transcriptomics we investigated lung gene expression responses to
MeSH term(s)	Age Factors ; Animals ; Bordetella Infections/genetics ; Bordetella Infections/immunology ; Bordetella pertussis/immunology ; Bordetella pertussis/pathogenicity ; Female ; Interferon Type I/genetics ; Interferon Type I/immunology ; Interferons/genetics ; Interferons/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Mutation ; Receptors, Interferon/deficiency ; Receptors, Interferon/genetics ; Receptors, Interferon/immunology ; Respiratory Tract Infections/genetics ; Respiratory Tract Infections/immunology ; Sequence Analysis, RNA ; Signal Transduction/genetics ; Signal Transduction/immunology ; Transcriptome ; Interferon Lambda
Chemical Substances	Interferon Type I ; Receptors, Interferon ; Interferons (9008-11-1) ; Interferon Lambda
Language	English
Publishing date	2020-03-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1900912
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