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Article ; Online: Morphogen-related therapeutic targets for liver fibrosis.

Fung, Eileen / Tsukamoto, Hidekazu

Clinics and research in hepatology and gastroenterology

2015 Volume 39 Suppl 1, Page(s) S69–74

Abstract: Recent research on hepatic stellate cells (HSCs) has spotlighted the involvement of morphogens in their cell fate determination in liver fibrosis. Temporally and spatially expressed during embryonic development, morphogens are involved in regulation of ... ...

Abstract	Recent research on hepatic stellate cells (HSCs) has spotlighted the involvement of morphogens in their cell fate determination in liver fibrosis. Temporally and spatially expressed during embryonic development, morphogens are involved in regulation of cell proliferation and differentiation, and tissue patterning. In normal adult liver, morphogens are generally expressed at low levels. However, in liver disease, myofibroblastic HSCs express morphogens such as Wnt, Shh, Necdin, DLK1, and Notch as part of their participation in fibrogenesis and wound healing. Liver regeneration involves cell proliferation and differentiation akin to embryonic liver development where the cells appear to undergo similar fates, and not surprisingly the morphogens are re-activated for the regenerative purpose in adult liver injury. Evidence also points to crosstalk of these morphogens in regulation of HSC fate determination. Genetic ablation or pharmacologic inhibition of morphogens reverts activated HSC to quiescent cells in culture and attenuates progression of hepatic fibrosis. However, positive regulation of liver regeneration by the morphogens needs to be spared. Therapeutically, manipulation of morphogen activities in a cell type and phase-specific manner should offer new modalities for chronic liver disease.
MeSH term(s)	Cell Transdifferentiation/physiology ; Hedgehog Proteins/physiology ; Hepatic Stellate Cells/physiology ; Humans ; Intercellular Signaling Peptides and Proteins/physiology ; Liver Cirrhosis/physiopathology ; Membrane Proteins/physiology ; Morphogenesis ; Nerve Tissue Proteins/physiology ; Nuclear Proteins/physiology ; Receptors, Notch/physiology ; Signal Transduction/physiology ; Wnt Signaling Pathway/physiology
Chemical Substances	DLK1 protein, human ; Hedgehog Proteins ; Intercellular Signaling Peptides and Proteins ; Membrane Proteins ; Nerve Tissue Proteins ; Nuclear Proteins ; Receptors, Notch ; necdin
Language	English
Publishing date	2015-09
Publishing country	France
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2594333-9
ISSN	2210-741X ; 2210-7401
ISSN (online)	2210-741X
ISSN	2210-7401
DOI	10.1016/j.clinre.2015.05.017
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Article: Glucose deprivation promotes pseudo-hypoxia and de-differentiation in lung adenocarcinoma.

Saggese, Pasquale / Pandey, Aparamita / Fung, Eileen / Hall, Abbie / Yanagawa, Jane / Rodriguez, Erika F / Grogan, Tristan R / Giurato, Giorgio / Nassa, Giovanni / Salvati, Annamaria / Weisz, Alessandro / Dubinett, Steven M / Scafoglio, Claudio

bioRxiv : the preprint server for biology

2023

Abstract: Increased utilization of glucose is a hallmark of cancer. Several studies are investigating the efficacy of glucose restriction by glucose transporter blockade or glycolysis inhibition. However, the adaptations of cancer cells to glucose restriction are ... ...

Abstract	Increased utilization of glucose is a hallmark of cancer. Several studies are investigating the efficacy of glucose restriction by glucose transporter blockade or glycolysis inhibition. However, the adaptations of cancer cells to glucose restriction are unknown. Here, we report the discovery that glucose restriction in lung adenocarcinoma (LUAD) induces cancer cell de-differentiation, leading to a more aggressive phenotype. Glucose deprivation causes a reduction in alpha-ketoglutarate (αKG), leading to attenuated activity of αKG-dependent histone demethylases and histone hypermethylation. We further show that this de-differentiated phenotype depends on unbalanced EZH2 activity, causing inhibition of prolyl-hydroxylase PHD3 and increased expression of hypoxia inducible factor 1α (HIF1α), triggering epithelial to mesenchymal transition. Finally, we identified an HIF1α-dependent transcriptional signature with prognostic significance in human LUAD. Our studies further current knowledge of the relationship between glucose metabolism and cell differentiation in cancer, characterizing the epigenetic adaptation of cancer cells to glucose deprivation and identifying novel targets to prevent the development of resistance to therapies targeting glucose metabolism.
Language	English
Publishing date	2023-02-01
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.01.30.526207
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Article ; Online: Glucose Deprivation Promotes Pseudohypoxia and Dedifferentiation in Lung Adenocarcinoma.

Saggese, Pasquale / Pandey, Aparamita / Alcaraz, Martín / Fung, Eileen / Hall, Abbie / Yanagawa, Jane / Rodriguez, Erika F / Grogan, Tristan R / Giurato, Giorgio / Nassa, Giovanni / Salvati, Annamaria / Shirihai, Orian S / Weisz, Alessandro / Dubinett, Steven M / Scafoglio, Claudio

Cancer research

2023 Volume 84, Issue 2, Page(s) 305–327

Abstract: Increased utilization of glucose is a hallmark of cancer. Sodium-glucose transporter 2 (SGLT2) is a critical player in glucose uptake in early-stage and well-differentiated lung adenocarcinoma (LUAD). SGLT2 inhibitors, which are FDA approved for diabetes, ...

Abstract	Increased utilization of glucose is a hallmark of cancer. Sodium-glucose transporter 2 (SGLT2) is a critical player in glucose uptake in early-stage and well-differentiated lung adenocarcinoma (LUAD). SGLT2 inhibitors, which are FDA approved for diabetes, heart failure, and kidney disease, have been shown to significantly delay LUAD development and prolong survival in murine models and in retrospective studies in diabetic patients, suggesting that they may be repurposed for lung cancer. Despite the antitumor effects of SGLT2 inhibition, tumors eventually escape treatment. Here, we studied the mechanisms of resistance to glucose metabolism-targeting treatments. Glucose restriction in LUAD and other tumors induced cancer cell dedifferentiation, leading to a more aggressive phenotype. Glucose deprivation caused a reduction in alpha-ketoglutarate (αKG), leading to attenuated activity of αKG-dependent histone demethylases and histone hypermethylation. The dedifferentiated phenotype depended on unbalanced EZH2 activity that suppressed prolyl-hydroxylase PHD3 and increased expression of hypoxia-inducible factor 1α (HIF1α), triggering epithelial-to-mesenchymal transition. Finally, a HIF1α-dependent transcriptional signature of genes upregulated by low glucose correlated with prognosis in human LUAD. Overall, this study furthers current knowledge of the relationship between glucose metabolism and cell differentiation in cancer, characterizing the epigenetic adaptation of cancer cells to glucose deprivation and identifying targets to prevent the development of resistance to therapies targeting glucose metabolism. Significance: Epigenetic adaptation allows cancer cells to overcome the tumor-suppressive effects of glucose restriction by inducing dedifferentiation and an aggressive phenotype, which could help design better metabolic treatments.
MeSH term(s)	Humans ; Mice ; Animals ; Glucose/metabolism ; Sodium-Glucose Transporter 2 ; Retrospective Studies ; Adenocarcinoma of Lung ; Lung Neoplasms/genetics
Chemical Substances	Glucose (IY9XDZ35W2) ; Sodium-Glucose Transporter 2
Language	English
Publishing date	2023-11-29
Publishing country	United States
Document type	Journal Article
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-23-1148
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Article: Pursuing Orally Bioavailable Hepcidin Analogues via Cyclic

Goncalves Monteiro, Daniela / van Dijk, Johannes W A / Aliyanto, Randy / Fung, Eileen / Nemeth, Elizabeta / Ganz, Tomas / Rosengren, Johan / Clark, Richard J

Biomedicines

2021 Volume 9, Issue 2

Abstract: The peptide hormone hepcidin is one of the key regulators of iron absorption, plasma iron levels, and tissue iron distribution. Hepcidin functions by binding to and inducing the internalisation and subsequent lysosomal degradation of ferroportin, which ... ...

Abstract	The peptide hormone hepcidin is one of the key regulators of iron absorption, plasma iron levels, and tissue iron distribution. Hepcidin functions by binding to and inducing the internalisation and subsequent lysosomal degradation of ferroportin, which reduces both iron absorption in the gut and export of iron from storage to ultimately decrease systemic iron levels. The key interaction motif in hepcidin has been localised to the highly conserved N-terminal region, comprising the first nine amino acid residues, and has led to the development of mini-hepcidin analogs that induce ferroportin internalisation and have improved drug-like properties. In this work, we have investigated the use of head-to-tail cyclisation and
Language	English
Publishing date	2021-02-08
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines9020164
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Article ; Online: Manipulation of the hepcidin pathway for therapeutic purposes.

Fung, Eileen / Nemeth, Elizabeta

Haematologica

2013 Volume 98, Issue 11, Page(s) 1667–1676

Abstract: Hepcidin, the liver-produced peptide hormone, is a principal regulator of iron homeostasis. Abnormal hepcidin production has emerged as a causative factor in several common iron disorders. Hepcidin insufficiency results in iron overload in hereditary ... ...

Abstract	Hepcidin, the liver-produced peptide hormone, is a principal regulator of iron homeostasis. Abnormal hepcidin production has emerged as a causative factor in several common iron disorders. Hepcidin insufficiency results in iron overload in hereditary hemochromatosis and iron-loading anemias, whereas hepcidin excess causes or contributes to the development of iron-restricted anemias in inflammatory diseases, infections, some cancers and chronic kidney disease. Not surprisingly, hepcidin and related pathways have become the target for the development of novel therapeutics for iron disorders. In this review, we will summarize the strategies and development programs that have been devised for agonizing or antagonizing hepcidin and its receptor ferroportin.
MeSH term(s)	Anemia, Iron-Deficiency/drug therapy ; Anemia, Iron-Deficiency/metabolism ; Animals ; Hepcidins/antagonists & inhibitors ; Hepcidins/metabolism ; Homeostasis/drug effects ; Homeostasis/physiology ; Humans ; Iron Chelating Agents/administration & dosage ; Iron Metabolism Disorders/drug therapy ; Iron Metabolism Disorders/metabolism ; Iron Overload/drug therapy ; Iron Overload/metabolism ; Signal Transduction/drug effects ; Signal Transduction/physiology
Chemical Substances	Hepcidins ; Iron Chelating Agents
Language	English
Publishing date	2013-11-05
Publishing country	Italy
Document type	Journal Article ; Review
ZDB-ID	2333-4
ISSN	1592-8721 ; 0017-6567 ; 0390-6078
ISSN (online)	1592-8721
ISSN	0017-6567 ; 0390-6078
DOI	10.3324/haematol.2013.084624
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Article: Mitoquinone mesylate targets SARS-CoV-2 infection in preclinical models.

Petcherski, Anton / Sharma, Madhav / Satta, Sandro / Daskou, Maria / Vasilopoulos, Hariclea / Hugo, Cristelle / Ritou, Eleni / Dillon, Barbara Jane / Fung, Eileen / Garcia, Gustavo / Scafoglio, Claudio / Purkayastha, Arunima / Gomperts, Brigitte N / Fishbein, Gregory A / Arumugaswami, Vaithilingaraja / Liesa, Marc / Shirihai, Orian S / Kelesidis, Theodoros

bioRxiv : the preprint server for biology

2022

Abstract: To date, there is no effective oral antiviral against SARS-CoV-2 that is also anti-inflammatory. Herein, we show that the mitochondrial antioxidant mitoquinone/mitoquinol mesylate (Mito-MES), a dietary supplement, has potent antiviral activity against ... ...

Abstract	To date, there is no effective oral antiviral against SARS-CoV-2 that is also anti-inflammatory. Herein, we show that the mitochondrial antioxidant mitoquinone/mitoquinol mesylate (Mito-MES), a dietary supplement, has potent antiviral activity against SARS-CoV-2 and its variants of concern One-sentence summary: Mitoquinone/mitoquinol mesylate has potent antiviral and anti-inflammatory activity in preclinical models of SARS-CoV-2 infection.
Language	English
Publishing date	2022-06-23
Publishing country	United States
Document type	Preprint
DOI	10.1101/2022.02.22.481100
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Article ; Online: In a Mouse Model of Sepsis, Hepcidin Ablation Ameliorates Anemia More Effectively than Iron and Erythropoietin Treatment.

Khorramian, Eeman / Fung, Eileen / Chua, Kristine / Gabayan, Victoria / Ganz, Tomas / Nemeth, Elizabeta / Kim, Airie

Shock (Augusta, Ga.)

2017 Volume 48, Issue 4, Page(s) 490–497

Abstract: Intensive care unit (ICU) anemia is an extreme version of anemia of inflammation that occurs commonly in critically ill patients and is associated with increased morbidity and mortality. Currently available therapies for ICU anemia have shown ... ...

Abstract	Intensive care unit (ICU) anemia is an extreme version of anemia of inflammation that occurs commonly in critically ill patients and is associated with increased morbidity and mortality. Currently available therapies for ICU anemia have shown inconsistent efficacies in clinical trials. We conducted a systematic study of the effects of early versus delayed iron (Fe) and/or erythropoietin (EPO) therapy in our previously characterized mouse model of ICU anemia based on an injection of heat-killed Brucella abortus. To study the effects of ongoing inflammation on the response to therapy, inflamed wild-type (WT) and hepcidin knockout (HKO) mice were treated at either early (days 1 and 2) or delayed (days 7 and 8) time points after the inflammatory stimulus. In the early treatment group, Fe and/or EPO therapy did not increase hemoglobin (Hgb) levels or reticulocyte production in either the inflamed WT or HKO groups. In the delayed treatment group, combination Fe + EPO therapy did increase Hgb and reticulocyte production in WT mice (mean ΔHgb in WT saline group -9.2 g/dL vs. Fe/EPO -5.5 g/dL; P < 0.001). The HKO mice in the delayed treatment group did not improve their Hgb, but HKO mice in all treatment groups developed a milder anemia than the WT mice. Our findings indicate that combination Fe + EPO therapy is effective in partially reversing ICU anemia when administered after the phase of acute inflammation. Hepcidin ablation alone was more effective in attenuating ICU anemia than Fe + EPO therapy, which indicates the potential of antihepcidin therapeutics in treating ICU anemia.
MeSH term(s)	Anemia/drug therapy ; Anemia/genetics ; Anemia/metabolism ; Anemia/pathology ; Animals ; Disease Models, Animal ; Erythropoietin/pharmacology ; Female ; Hepcidins/antagonists & inhibitors ; Hepcidins/genetics ; Iron/pharmacology ; Male ; Mice ; Mice, Knockout ; Sepsis/drug therapy ; Sepsis/genetics ; Sepsis/metabolism ; Sepsis/pathology
Chemical Substances	Hepcidins ; Erythropoietin (11096-26-7) ; Iron (E1UOL152H7)
Language	English
Publishing date	2017-06-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	1185432-7
ISSN	1540-0514 ; 1073-2322
ISSN (online)	1540-0514
ISSN	1073-2322
DOI	10.1097/SHK.0000000000000886
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Article ; Online: Single-Cell Characterization of Pulmonary Nodules Implicates Suppression of Immunosurveillance across Early Stages of Lung Adenocarcinoma.

Cancer research

2023 Volume 83, Issue 19, Page(s) 3305–3319

Abstract: A greater understanding of molecular, cellular, and immunological changes during the early stages of lung adenocarcinoma development could improve diagnostic and therapeutic approaches in patients with pulmonary nodules at risk for lung cancer. To ... ...

Abstract	A greater understanding of molecular, cellular, and immunological changes during the early stages of lung adenocarcinoma development could improve diagnostic and therapeutic approaches in patients with pulmonary nodules at risk for lung cancer. To elucidate the immunopathogenesis of early lung tumorigenesis, we evaluated surgically resected pulmonary nodules representing the spectrum of early lung adenocarcinoma as well as associated normal lung tissues using single-cell RNA sequencing and validated the results by flow cytometry and multiplex immunofluorescence (MIF). Single-cell transcriptomics revealed a significant decrease in gene expression associated with cytolytic activities of tumor-infiltrating natural killer and natural killer T cells. This was accompanied by a reduction in effector T cells and an increase of CD4+ regulatory T cells (Treg) in subsolid nodules. An independent set of resected pulmonary nodules consisting of both adenocarcinomas and associated premalignant lesions corroborated the early increment of Tregs in premalignant lesions compared with the associated normal lung tissues by MIF. Gene expression analysis indicated that cancer-associated alveolar type 2 cells and fibroblasts may contribute to the deregulation of the extracellular matrix, potentially affecting immune infiltration in subsolid nodules through ligand-receptor interactions. These findings suggest that there is a suppression of immune surveillance across the spectrum of early-stage lung adenocarcinoma. Significance: Analysis of a spectrum of subsolid pulmonary nodules by single-cell RNA sequencing provides insights into the immune regulation and cell-cell interactions in the tumor microenvironment during early lung tumor development.
MeSH term(s)	Humans ; Monitoring, Immunologic ; Tomography, X-Ray Computed/methods ; Adenocarcinoma of Lung/genetics ; Adenocarcinoma of Lung/pathology ; Lung Neoplasms/pathology ; Multiple Pulmonary Nodules ; Adenocarcinoma/genetics ; Adenocarcinoma/pathology ; Tumor Microenvironment
Language	English
Publishing date	2023-10-31
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-23-0128
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Article ; Online: Thiol-derivatized minihepcidins retain biological activity.

Fung, Eileen / Chua, Kristine / Ganz, Tomas / Nemeth, Elizabeta / Ruchala, Piotr

Bioorganic & medicinal chemistry letters

2015 Volume 25, Issue 4, Page(s) 763–766

Abstract: Minihepcidins are small peptides that mimic biological activity of the iron-regulatory hormone hepcidin. Structurally, they contain thiol-free-cysteine residue in position 7 which is crucial for their bioactivity. Nonetheless, free sulfhydryl group is ... ...

Abstract	Minihepcidins are small peptides that mimic biological activity of the iron-regulatory hormone hepcidin. Structurally, they contain thiol-free-cysteine residue in position 7 which is crucial for their bioactivity. Nonetheless, free sulfhydryl group is not desirable in pharmaceutical entities as it may lead to dermatological side effects. Moreover free thiol moiety is quite reactive and depending on conditions/reagents may be alkylated and/or oxidized giving various Cys-derivatives: S-alkyl cysteines, sulfoxides, sulfones, disulfides, cysteinesulfinic and cysteic acids. To limit such reactivity and maintain bioactivity of minihepcidin(s) we used thiol-protection strategy based on activated vinyl thioethers. Novel S-protected analogs of physiologically active minihepcidin PR73 were synthesized and tested in vitro showing activity comparable to parental molecule. The most active compound, PR73SH was also tested in vivo showing activity profile analogous to PR73. Collectively, our findings suggest that S-vinyl-derivatization of minihepcidin(s) may be a suitable approach in the development of physiologically active agonists of hepcidin.
MeSH term(s)	Biomimetic Materials/chemistry ; Biomimetic Materials/pharmacology ; Hepcidins/chemistry ; Hepcidins/pharmacology ; Iron/chemistry ; Peptides/chemistry ; Peptides/pharmacology ; Structure-Activity Relationship ; Sulfhydryl Compounds/chemistry ; Sulfhydryl Compounds/pharmacology
Chemical Substances	Hepcidins ; Peptides ; Sulfhydryl Compounds ; Iron (E1UOL152H7)
Language	English
Publishing date	2015-02-15
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1063195-1
ISSN	1464-3405 ; 0960-894X
ISSN (online)	1464-3405
ISSN	0960-894X
DOI	10.1016/j.bmcl.2014.12.094
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Article ; Online: Small cyclic agonists of iron regulatory hormone hepcidin.

Chua, Kristine / Fung, Eileen / Micewicz, Ewa D / Ganz, Tomas / Nemeth, Elizabeta / Ruchala, Piotr

Bioorganic & medicinal chemistry letters

2015 Volume 25, Issue 21, Page(s) 4961–4969

Abstract: Minihepcidins are in vitro and in vivo active mimetics of iron-regulatory hormone hepcidin. They contain various unusual amino acids including: N-substituted, β-homo-, and d-amino acids with their combination depending on particular minihepcidin. In the ... ...

Abstract	Minihepcidins are in vitro and in vivo active mimetics of iron-regulatory hormone hepcidin. They contain various unusual amino acids including: N-substituted, β-homo-, and d-amino acids with their combination depending on particular minihepcidin. In the current study, we sought to limit the use of unusual/more expensive amino acids derivatives by peptide cyclization. Novel cyclic mimetics of hepcidin were synthesized and tested in vitro and showed activity at low nanomolar concentration. Nonetheless, the most active cyclic compound (mHS17) is approximately ten times less active than the parental minihepcidin PR73. Collectively, our findings suggest that cyclization is viable approach in the synthesis of hepcidin mimetics.
MeSH term(s)	Amino Acids/chemistry ; Amino Acids/pharmacology ; Dose-Response Relationship, Drug ; Hepcidins/agonists ; Humans ; Molecular Structure ; Peptides/chemical synthesis ; Peptides/chemistry ; Peptides/pharmacology ; Structure-Activity Relationship
Chemical Substances	Amino Acids ; Hepcidins ; Peptides
Language	English
Publishing date	2015-03-12
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1063195-1
ISSN	1464-3405 ; 0960-894X
ISSN (online)	1464-3405
ISSN	0960-894X
DOI	10.1016/j.bmcl.2015.03.012
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