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Article ; Online: From the Inside Out: Exposing the Roles of Urea Cycle Enzymes in Tumors and Their Micro and Macro Environments.

Hajaj, Emma / Pozzi, Sabina / Erez, Ayelet

Cold Spring Harbor perspectives in medicine

2024 Volume 14, Issue 4

Abstract: Catabolic pathways change in anabolic diseases such as cancer to maintain metabolic homeostasis. The liver urea cycle (UC) is the main catabolic pathway for disposing excess nitrogen. Outside the liver, the UC enzymes are differentially expressed based ... ...

Abstract	Catabolic pathways change in anabolic diseases such as cancer to maintain metabolic homeostasis. The liver urea cycle (UC) is the main catabolic pathway for disposing excess nitrogen. Outside the liver, the UC enzymes are differentially expressed based on each tissue's needs for UC intermediates. In tumors, there are changes in the expression of UC enzymes selected for promoting tumorigenesis by increasing the availability of essential UC substrates and products. Consequently, there are compensatory changes in the expression of UC enzymes in the cells that compose the tumor microenvironment. Moreover, extrahepatic tumors induce changes in the expression of the liver UC, which contribute to the systemic manifestations of cancer, such as weight loss. Here, we review the multilayer changes in the expression of UC enzymes throughout carcinogenesis. Understanding the changes in UC expression in the tumor and its micro and macro environment can help identify biomarkers for early cancer diagnosis and vulnerabilities that can be targeted for therapy.
MeSH term(s)	Humans ; Neoplasms/metabolism ; Liver/metabolism ; Urea/metabolism ; Tumor Microenvironment
Chemical Substances	Urea (8W8T17847W)
Language	English
Publishing date	2024-04-01
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2157-1422
ISSN (online)	2157-1422
DOI	10.1101/cshperspect.a041538
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The context-specific roles of urea cycle enzymes in tumorigenesis.

Hajaj, Emma / Sciacovelli, Marco / Frezza, Christian / Erez, Ayelet

Molecular cell

2021 Volume 81, Issue 18, Page(s) 3749–3759

Abstract: The expression of the urea cycle (UC) proteins is dysregulated in multiple cancers, providing metabolic benefits to tumor survival, proliferation, and growth. Here, we review the main changes described in the expression of UC enzymes and metabolites in ... ...

Abstract	The expression of the urea cycle (UC) proteins is dysregulated in multiple cancers, providing metabolic benefits to tumor survival, proliferation, and growth. Here, we review the main changes described in the expression of UC enzymes and metabolites in different cancers at various stages and suggest that these changes are dynamic and should hence be viewed in a context-specific manner. Understanding the evolvability in the activity of the UC pathway in cancer has implications for cancer-immune cell interactions and for cancer diagnosis and therapy.
MeSH term(s)	Ammonia/metabolism ; Carcinogenesis/metabolism ; Cell Line, Tumor ; Cell Proliferation ; Cell Transformation, Neoplastic/metabolism ; Gene Expression/genetics ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic/genetics ; Humans ; Urea/metabolism ; Urea Cycle Disorders, Inborn/metabolism ; Urea Cycle Disorders, Inborn/physiopathology
Chemical Substances	Ammonia (7664-41-7) ; Urea (8W8T17847W)
Language	English
Publishing date	2021-08-31
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2021.08.005
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Article ; Online: Argininosuccinic aciduria: from a monogenic to a complex disorder.

Erez, Ayelet

Genetics in medicine : official journal of the American College of Medical Genetics

2013 Volume 15, Issue 4, Page(s) 251–257

Abstract: In the early 1930s, phenylketonuria was among the first metabolic diseases to be defined. In the following years, multiple attempts to correlate genotype and phenotype in several inherited metabolic diseases, including phenylketonuria, were encountered ... ...

Abstract	In the early 1930s, phenylketonuria was among the first metabolic diseases to be defined. In the following years, multiple attempts to correlate genotype and phenotype in several inherited metabolic diseases, including phenylketonuria, were encountered with difficulties. It is becoming evident that the phenotype of metabolic disorders is often more multifaceted than expected from the disruption of a specific enzyme function caused by a single-gene disorder. Undoubtedly, revealing the factors contributing to the discrepancy between the loss of a single enzymatic function and the wide spectrum of clinical consequences would allow clinicians to optimize treatment for their patients. This article discusses several possible contributors to the unique, complex phenotypes observed in inherited metabolic disorders, using argininosuccinic aciduria as a disease model.Genet Med 2013:15(4):251-257.
MeSH term(s)	Animals ; Argininosuccinic Aciduria/genetics ; Argininosuccinic Aciduria/metabolism ; Enzymes/chemistry ; Enzymes/genetics ; Enzymes/metabolism ; Humans ; Metabolic Networks and Pathways ; Mutation ; Phenotype
Chemical Substances	Enzymes
Language	English
Publishing date	2013-01-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1455352-1
ISSN	1530-0366 ; 1098-3600
ISSN (online)	1530-0366
ISSN	1098-3600
DOI	10.1038/gim.2012.166
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Article ; Online: Targeting Metabolic Plasticity and Flexibility Dynamics for Cancer Therapy.

Fendt, Sarah-Maria / Frezza, Christian / Erez, Ayelet

Cancer discovery

2020 Volume 10, Issue 12, Page(s) 1797–1807

Abstract: Cancer cells continuously rewire their metabolism to fulfill their need for rapid growth and survival while subject to changes in environmental cues. Thus, a vital component of a cancer cell lies in its metabolic adaptability. The constant demand for ... ...

Abstract	Cancer cells continuously rewire their metabolism to fulfill their need for rapid growth and survival while subject to changes in environmental cues. Thus, a vital component of a cancer cell lies in its metabolic adaptability. The constant demand for metabolic alterations requires flexibility, that is, the ability to utilize different metabolic substrates; as well as plasticity, that is, the ability to process metabolic substrates in different ways. In this review, we discuss how dynamic changes in cancer metabolism affect tumor progression and the consequential implications for cancer therapy. SIGNIFICANCE: Recognizing cancer dynamic metabolic adaptability as an entity can lead to targeted therapy that is expected to decrease drug resistance.
MeSH term(s)	Humans ; Neoplasms/therapy ; Tumor Microenvironment/genetics
Language	English
Publishing date	2020-11-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2625242-9
ISSN	2159-8290 ; 2159-8274
ISSN (online)	2159-8290
ISSN	2159-8274
DOI	10.1158/2159-8290.CD-20-0844
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Article: The context-specific roles of urea cycle enzymes in tumorigenesis

Hajaj, Emma / Sciacovelli, Marco / Frezza, Christian / Erez, Ayelet

Molecular cell. 2021 Sept. 16, v. 81, no. 18

2021

Abstract	The expression of the urea cycle (UC) proteins is dysregulated in multiple cancers, providing metabolic benefits to tumor survival, proliferation, and growth. Here, we review the main changes described in the expression of UC enzymes and metabolites in different cancers at various stages and suggest that these changes are dynamic and should hence be viewed in a context-specific manner. Understanding the evolvability in the activity of the UC pathway in cancer has implications for cancer-immune cell interactions and for cancer diagnosis and therapy.
Keywords	carcinogenesis ; metabolites ; neoplasms ; therapeutics ; urea cycle
Language	English
Dates of publication	2021-0916
Size	p. 3749-3759.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2021.08.005
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Arginine and the metabolic regulation of nitric oxide synthesis in cancer.

Keshet, Rom / Erez, Ayelet

Disease models & mechanisms

2018 Volume 11, Issue 8

Abstract: Nitric oxide (NO) is a signaling molecule that plays important roles in diverse biological processes and thus its dysregulation is involved in the pathogenesis of various disorders. In cancer, NO has broad and sometimes dichotomous roles; it is involved ... ...

Abstract	Nitric oxide (NO) is a signaling molecule that plays important roles in diverse biological processes and thus its dysregulation is involved in the pathogenesis of various disorders. In cancer, NO has broad and sometimes dichotomous roles; it is involved in cancer initiation and progression, but also restricts cancer proliferation and invasion, and contributes to the anti-tumor immune response. The importance of NO in a range of cellular processes is exemplified by its tight spatial and dosage control at multiple levels, including via its transcriptional, post-translational and metabolic regulation. In this Review, we focus on the regulation of NO via the synthesis and availability of its precursor, arginine, and discuss the implications of this metabolic regulation for cancer biology and therapy. Despite the established contribution of NO to cancer pathogenesis, the implementation of NO-related cancer therapeutics remains limited, likely due to the challenge of targeting and inducing its protective functions in a cell- and dosage-specific manner. A better understanding of how arginine regulates the production of NO in cancer might thus support the development of anti-cancer drugs that target this key metabolic pathway, and other metabolic pathways involved in NO production.
MeSH term(s)	Animals ; Antineoplastic Agents/therapeutic use ; Arginine/metabolism ; Humans ; Models, Biological ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Nitric Oxide/biosynthesis
Chemical Substances	Antineoplastic Agents ; Nitric Oxide (31C4KY9ESH) ; Arginine (94ZLA3W45F)
Language	English
Publishing date	2018-08-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	1754-8411
ISSN (online)	1754-8411
DOI	10.1242/dmm.033332
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Arginine and the metabolic regulation of nitric oxide synthesis in cancer

Rom Keshet / Ayelet Erez

Disease Models & Mechanisms, Vol 11, Iss

2018 Volume 8

Abstract	Nitric oxide (NO) is a signaling molecule that plays important roles in diverse biological processes and thus its dysregulation is involved in the pathogenesis of various disorders. In cancer, NO has broad and sometimes dichotomous roles; it is involved in cancer initiation and progression, but also restricts cancer proliferation and invasion, and contributes to the anti-tumor immune response. The importance of NO in a range of cellular processes is exemplified by its tight spatial and dosage control at multiple levels, including via its transcriptional, post-translational and metabolic regulation. In this Review, we focus on the regulation of NO via the synthesis and availability of its precursor, arginine, and discuss the implications of this metabolic regulation for cancer biology and therapy. Despite the established contribution of NO to cancer pathogenesis, the implementation of NO-related cancer therapeutics remains limited, likely due to the challenge of targeting and inducing its protective functions in a cell- and dosage-specific manner. A better understanding of how arginine regulates the production of NO in cancer might thus support the development of anti-cancer drugs that target this key metabolic pathway, and other metabolic pathways involved in NO production.
Keywords	Nitric oxide metabolism ; Arginine ; Cancer metabolism ; Medicine ; R ; Pathology ; RB1-214
Subject code	570
Language	English
Publishing date	2018-08-01T00:00:00Z
Publisher	The Company of Biologists
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: From Prokaryotes to Cancer: Glutamine Flux in Multicellular Units.

Erez, Ayelet / Kolodkin-Gal, Ilana

Trends in endocrinology and metabolism: TEM

2017 Volume 28, Issue 9, Page(s) 637–644

Abstract: Bacteria in nature reside in organized communities, termed biofilms, which are composed of multiple individual cells adhering to each other. Similarly, tumors are a multicellular mass with distinct cellular phenotypes. Both tumors and biofilms are ... ...

Abstract	Bacteria in nature reside in organized communities, termed biofilms, which are composed of multiple individual cells adhering to each other. Similarly, tumors are a multicellular mass with distinct cellular phenotypes. Both tumors and biofilms are considered to be an active interphase between unicellular and multicellular life states. Because both of these units depend on glutamine for growth and survival, we review here glutamine flux within them as a readout for intra- and inter-commensal metabolism. We suggest that the difference between glutamine fluxes in these cellular communities lies mainly in their global multicellular metabolic organization. Both the differences and similarities described here should be taken into account when considering glutamine-targeting therapeutic approaches.
Language	English
Publishing date	2017-09
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1042384-9
ISSN	1879-3061 ; 1043-2760
ISSN (online)	1879-3061
ISSN	1043-2760
DOI	10.1016/j.tem.2017.05.007
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Zs.A 2999: Show issues

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Article ; Online: The Clinical Significance of LDL-Cholesterol on the Outcomes of Hemodialysis Patients with Acute Coronary Syndrome.

Cohen-Hagai, Keren / Benchetrit, Sydney / Wand, Ori / Grupper, Ayelet / Shashar, Moshe / Solo, Olga / Pereg, David / Zitman-Gal, Tali / Haskiah, Feras / Erez, Daniel

Medicina (Kaunas, Lithuania)

2023 Volume 59, Issue 7

Abstract: Background and ... ...

Abstract	Background and objectives
MeSH term(s)	Humans ; Cholesterol, LDL ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use ; Acute Coronary Syndrome/complications ; Acute Coronary Syndrome/epidemiology ; Clinical Relevance ; Retrospective Studies ; Renal Dialysis/adverse effects ; Inflammation/drug therapy
Chemical Substances	Cholesterol, LDL ; Hydroxymethylglutaryl-CoA Reductase Inhibitors
Language	English
Publishing date	2023-07-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2188113-3
ISSN	1648-9144 ; 1010-660X
ISSN (online)	1648-9144
ISSN	1010-660X
DOI	10.3390/medicina59071312
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Article: A metabolic link between the urea cycle and cancer cell proliferation.

Nagamani, Sandesh C S / Erez, Ayelet

Molecular & cellular oncology

2016 Volume 3, Issue 2, Page(s) e1127314

Abstract: Clinical observations in citrullinemia type I, an inborn error of metabolism, led us to explore the benefits of somatic ASS1 silencing in cancer. We found that downregulation of ASS1 results in preferential utilization of its substrate, aspartate, for ... ...

Abstract	Clinical observations in citrullinemia type I, an inborn error of metabolism, led us to explore the benefits of somatic ASS1 silencing in cancer. We found that downregulation of ASS1 results in preferential utilization of its substrate, aspartate, for pyrimidine synthesis to support cell proliferation. Reducing aspartate availability for pyrimidine synthesis restricted cancerous proliferation.
Language	English
Publishing date	2016-02-18
Publishing country	United States
Document type	Journal Article
ISSN	2372-3556
ISSN	2372-3556
DOI	10.1080/23723556.2015.1127314
Database	MEDical Literature Analysis and Retrieval System OnLINE

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