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Article: Targeting cancer energy metabolism: a potential systemic cure for cancer.

Kim, Soo-Youl

2019 Volume 42, Issue 2, Page(s) 140–149

Abstract: Long-term investigation and extensive efforts using sequencing and -omics analysis identified thousands of mutations in a single tumor. However, we cannot succeed at curing cancer by targeting mutations as the cause of cancer. Therefore, as an alternate ... ...

Abstract	Long-term investigation and extensive efforts using sequencing and -omics analysis identified thousands of mutations in a single tumor. However, we cannot succeed at curing cancer by targeting mutations as the cause of cancer. Therefore, as an alternate therapeutic approach from classical oncology study, stimulation of the inherent ability of the immune system to attack tumor cells was welcome as a new principle in cancer therapy. However, it cannot be a permanent solution for the question of "which is the common factor that can distinguish cancer from normal?" Targeting the cancer energy metabolism may be a cancer-specific therapy for all kinds of cancer because normal cells do not rely on cancer energy metabolism under normal conditions. Here, trends of cancer metabolism as well as a new theory of cancer energy metabolism in the therapeutic approach is summarized.
MeSH term(s)	Animals ; Antineoplastic Agents/administration & dosage ; Drug Delivery Systems/methods ; Drug Delivery Systems/trends ; Energy Metabolism/drug effects ; Energy Metabolism/physiology ; Glucose/antagonists & inhibitors ; Glucose/metabolism ; Glycolysis/drug effects ; Glycolysis/physiology ; Humans ; Neoplasms/drug therapy ; Neoplasms/metabolism
Chemical Substances	Antineoplastic Agents ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2019-01-17
Publishing country	Korea (South)
Document type	Journal Article ; Review
ZDB-ID	447623-2
ISSN	1976-3786 ; 0253-6269
ISSN (online)	1976-3786
ISSN	0253-6269
DOI	10.1007/s12272-019-01115-2
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Article ; Online: New Insights into Development of Transglutaminase 2 Inhibitors as Pharmaceutical Lead Compounds.

Kim, Soo-Youl

Medical sciences (Basel, Switzerland)

2018 Volume 6, Issue 4

Abstract: Transglutaminase 2 (EC 2.3.2.13; TG2 or TGase 2) plays important roles in the pathogenesis of many diseases, including cancers, neurodegeneration, and inflammatory disorders. Under normal conditions, however, mice lacking TGase 2 exhibit no obvious ... ...

Abstract	Transglutaminase 2 (EC 2.3.2.13; TG2 or TGase 2) plays important roles in the pathogenesis of many diseases, including cancers, neurodegeneration, and inflammatory disorders. Under normal conditions, however, mice lacking TGase 2 exhibit no obvious abnormal phenotype. TGase 2 expression is induced by chemical, physical, and viral stresses through tissue-protective signaling pathways. After stress dissipates, expression is normalized by feedback mechanisms. Dysregulation of TGase 2 expression under pathologic conditions, however, can potentiate pathogenesis and aggravate disease severity. Consistent with this, TGase 2 knockout mice exhibit reversal of disease phenotypes in neurodegenerative and chronic inflammatory disease models. Accordingly, TGase 2 is considered to be a potential therapeutic target. Based on structure⁻activity relationship assays performed over the past few decades, TGase 2 inhibitors have been developed that target the enzyme's active site, but clinically applicable inhibitors are not yet available. The recently described the small molecule GK921, which lacks a group that can react with the active site of TGase 2, and efficiently inhibits the enzyme's activity. Mechanistic studies revealed that GK921 binds at an allosteric binding site in the N-terminus of TGase 2 (amino acids (a.a.) 81⁻116), triggering a conformational change that inactivates the enzyme. Because the binding site of GK921 overlaps with the p53-binding site of TGase 2, the drug induces apoptosis in renal cell carcinoma by stabilizing p53. In this review, we discuss the possibility of developing TGase 2 inhibitors that target the allosteric binding site of TGase 2.
Language	English
Publishing date	2018-10-08
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2754473-4
ISSN	2076-3271 ; 2076-3271
ISSN (online)	2076-3271
ISSN	2076-3271
DOI	10.3390/medsci6040087
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Article: Cancer Energy Metabolism: Shutting Power off Cancer Factory.

Kim, Soo-Youl

Biomolecules & therapeutics

2017 Volume 26, Issue 1, Page(s) 39–44

Abstract: In 1923, Dr. Warburg had observed that tumors acidified the Ringer solution when 13 mM glucose was added, which was identified as being due to lactate. When glucose is the only source of nutrient, it can serve for both biosynthesis and energy production. ...

Abstract	In 1923, Dr. Warburg had observed that tumors acidified the Ringer solution when 13 mM glucose was added, which was identified as being due to lactate. When glucose is the only source of nutrient, it can serve for both biosynthesis and energy production. However, a series of studies revealed that the cancer cell consumes glucose for biosynthesis through fermentation, not for energy supply, under physiological conditions. Recently, a new observation was made that there is a metabolic symbiosis in which glycolytic and oxidative tumor cells mutually regulate their energy metabolism. Hypoxic cancer cells use glucose for glycolytic metabolism and release lactate which is used by oxygenated cancer cells. This study challenged the Warburg effect, because Warburg claimed that fermentation by irreversible damaging of mitochondria is a fundamental cause of cancer. However, recent studies revealed that mitochondria in cancer cell show active function of oxidative phosphorylation although TCA cycle is stalled. It was also shown that blocking cytosolic NADH production by aldehyde dehydrogenase inhibition, combined with oxidative phosphorylation inhibition, resulted in up to 80% decrease of ATP production, which resulted in a significant regression of tumor growth in the NSCLC model. This suggests a new theory that NADH production in the cytosol plays a key role of ATP production through the mitochondrial electron transport chain in cancer cells, while NADH production is mostly occupied inside mitochondria in normal cells.
Language	English
Publishing date	2017-12-12
Publishing country	Korea (South)
Document type	Journal Article ; Review
ZDB-ID	2734146-X
ISSN	2005-4483 ; 1976-9148
ISSN (online)	2005-4483
ISSN	1976-9148
DOI	10.4062/biomolther.2017.184
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Article: Cancer Metabolism: a Hope for Curing Cancer.

Kim, Soo-Youl

Biomolecules & therapeutics

2017 Volume 26, Issue 1, Page(s) 1–3

Language	English
Publishing date	2017-12-12
Publishing country	Korea (South)
Document type	Journal Article
ZDB-ID	2734146-X
ISSN	2005-4483 ; 1976-9148
ISSN (online)	2005-4483
ISSN	1976-9148
DOI	10.4062/biomolther.2017.300
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Article ; Online: A Precision Strategy to Cure Renal Cell Carcinoma by Targeting Transglutaminase 2.

Kim, Soo-Youl / Keillor, Jeffrey W

International journal of molecular sciences

2020 Volume 21, Issue 7

Abstract: In a recent report, no significance of transglutaminase 2 (TGase 2) was noted in the analyses of expression differences between normal and clear cell renal cell carcinoma (ccRCC), although we found that knock down of TGase 2 induced significant p53- ... ...

Abstract	In a recent report, no significance of transglutaminase 2 (TGase 2) was noted in the analyses of expression differences between normal and clear cell renal cell carcinoma (ccRCC), although we found that knock down of TGase 2 induced significant p53-mediated cell death in ccRCC. Generally, to find effective therapeutic targets, we need to identify targets that belong specifically to a cancer phenotype that can be differentiated from a normal phenotype. Here, we offer precise reasons why TGase 2 may be the first therapeutic target for ccRCC, according to several lines of evidence. TGase 2 is negatively regulated by von Hippel-Lindau tumor suppressor protein (pVHL) and positively regulated by hypoxia-inducible factor 1-α (HIF-1α in renal cell carcinoma (RCC). Therefore, most of ccRCC presents high level expression of TGase 2 because over 90% of ccRCC showed
MeSH term(s)	Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Carcinoma, Renal Cell/drug therapy ; Carcinoma, Renal Cell/genetics ; Carcinoma, Renal Cell/metabolism ; Drug Resistance, Neoplasm ; GTP-Binding Proteins/drug effects ; GTP-Binding Proteins/genetics ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Kidney Neoplasms/drug therapy ; Kidney Neoplasms/genetics ; Kidney Neoplasms/metabolism ; Molecular Targeted Therapy ; Precision Medicine ; Transglutaminases/drug effects ; Transglutaminases/genetics ; Tumor Suppressor Protein p53/metabolism ; Von Hippel-Lindau Tumor Suppressor Protein/genetics ; Von Hippel-Lindau Tumor Suppressor Protein/metabolism
Chemical Substances	Antineoplastic Agents ; HIF1A protein, human ; Hypoxia-Inducible Factor 1, alpha Subunit ; TP53 protein, human ; Tumor Suppressor Protein p53 ; transglutaminase 2 (EC 2.3.2.-) ; Transglutaminases (EC 2.3.2.13) ; Von Hippel-Lindau Tumor Suppressor Protein (EC 2.3.2.27) ; GTP-Binding Proteins (EC 3.6.1.-) ; VHL protein, human (EC 6.3.2.-)
Language	English
Publishing date	2020-04-03
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21072493
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Article: Cancer metabolism: strategic diversion from targeting cancer drivers to targeting cancer suppliers.

Kim, Soo-Youl

Biomolecules & therapeutics

2015 Volume 23, Issue 2, Page(s) 99–109

Abstract: Drug development groups are close to discovering another pot of gold-a therapeutic target-similar to the success of imatinib (Gleevec) in the field of cancer biology. Modern molecular biology has improved cancer therapy through the identification of more ...

Abstract	Drug development groups are close to discovering another pot of gold-a therapeutic target-similar to the success of imatinib (Gleevec) in the field of cancer biology. Modern molecular biology has improved cancer therapy through the identification of more pharmaceutically viable targets, and yet major problems and risks associated with late-phase cancer therapy remain. Presently, a growing number of reports have initiated a discussion about the benefits of metabolic regulation in cancers. The Warburg effect, a great discovery approximately 70 years ago, addresses the "universality" of cancer characteristics. For instance, most cancer cells prefer aerobic glycolysis instead of mitochondrial respiration. Recently, cancer metabolism has been explained not only by metabolites but also through modern molecular and chemical biological techniques. Scientists are seeking context-dependent universality among cancer types according to metabolic and enzymatic pathway signatures. This review presents current cancer metabolism studies and discusses future directions in cancer therapy targeting bio-energetics, bio-anabolism, and autophagy, emphasizing the important contribution of cancer metabolism in cancer therapy.
Language	English
Publishing date	2015-03-01
Publishing country	Korea (South)
Document type	Journal Article ; Review
ZDB-ID	2734146-X
ISSN	2005-4483 ; 1976-9148
ISSN (online)	2005-4483
ISSN	1976-9148
DOI	10.4062/biomolther.2015.013
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Article: Cancer metabolism: targeting cancer universality.

Kim, Soo-Youl

Archives of pharmacal research

2015 Volume 38, Issue 3, Page(s) 299–301

Abstract: Cancer metabolism has taken a step forward lately using modern molecular and chemical biology techniques. The future direction will most likely be defined by scientists looking for the commonality between cancer types, using metabolic gene signatures, ... ...

Abstract	Cancer metabolism has taken a step forward lately using modern molecular and chemical biology techniques. The future direction will most likely be defined by scientists looking for the commonality between cancer types, using metabolic gene signatures, RNA and protein signatures of metabolic enzymes. Cancer metabolism may be the missing link between the inductive and deductive methods in the scientific method.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Humans ; Molecular Targeted Therapy ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/metabolism
Chemical Substances	Antineoplastic Agents
Language	English
Publishing date	2015-03
Publishing country	Korea (South)
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	447623-2
ISSN	1976-3786 ; 0253-6269
ISSN (online)	1976-3786
ISSN	0253-6269
DOI	10.1007/s12272-015-0551-5
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Article ; Online: Special issues from High 1: KSBMB Winter Workshop.

Kim, Soo-Youl

BMB reports

2014 Volume 47, Issue 3, Page(s) 121

MeSH term(s)	Biochemistry ; Congresses as Topic ; Drug Discovery ; Korea ; Molecular Biology ; Molecular Probes/metabolism ; Molecular Targeted Therapy ; Proteomics ; Seasons ; Societies, Scientific ; Stem Cell Research ; Translational Medical Research
Chemical Substances	Molecular Probes
Language	English
Publishing date	2014-03-30
Publishing country	Korea (South)
Document type	Editorial ; Introductory Journal Article
ZDB-ID	2410389-5
ISSN	1976-670X ; 1976-6696
ISSN (online)	1976-670X
ISSN	1976-6696
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Article ; Online: Cancer depends on fatty acids for ATP production: A possible link between cancer and obesity.

Lee, Ho / Woo, Sang Myung / Jang, Hyonchol / Kang, Mingyu / Kim, Soo-Youl

Seminars in cancer biology

2022 Volume 86, Issue Pt 2, Page(s) 347–357

Abstract: Several metabolic pathways for the supply of adenosine triphosphate (ATP) have been proposed; however, the major source of reducing power for ADP in cancer remains unclear. Although glycolysis is the source of ATP in tumors according to the Warburg ... ...

Abstract	Several metabolic pathways for the supply of adenosine triphosphate (ATP) have been proposed; however, the major source of reducing power for ADP in cancer remains unclear. Although glycolysis is the source of ATP in tumors according to the Warburg effect, ATP levels do not differ between cancer cells grown in the presence and absence of glucose. Several theories have been proposed to explain the supply of ATP in cancer, including metabolic reprograming in the tumor microenvironment. However, these theories are based on the production of ATP by the TCA-OxPhos pathway, which is inconsistent with the Warburg effect. We found that blocking fatty acid oxidation (FAO) in the presence of glucose significantly decreased ATP production in various cancer cells. This suggests that cancer cells depend on fatty acids to produce ATP through FAO instead of glycolysis. We observed that cancer cell growth mainly relies on metabolic nutrients and oxygen systemically supplied through the bloodstream instead of metabolic reprogramming. In a spontaneous mouse tumor model (Kras<sup>G12D</sup>; Pdx1-cre), tumor growth was 2-fold higher in mice fed a high-fat diet (low-carbo diet) that caused obesity, whereas a calorie-balanced, low-fat diet (high-carbo diet) inhibited tumor growth by 3-fold compared with that in mice fed a control/normal diet. This 5-fold difference in tumor growth between mice fed low-fat and high-fat diets suggests that fat-induced obesity promotes cancer growth, and tumor growth depends on fatty acids as the primary source of energy.
MeSH term(s)	Mice ; Humans ; Animals ; Fatty Acids/metabolism ; Adenosine Triphosphate/metabolism ; Diet, High-Fat ; Obesity/complications ; Obesity/metabolism ; Glucose/metabolism ; Neoplasms/etiology ; Tumor Microenvironment
Chemical Substances	Fatty Acids ; Adenosine Triphosphate (8L70Q75FXE) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2022-07-19
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	1033980-2
ISSN	1096-3650 ; 1044-579X
ISSN (online)	1096-3650
ISSN	1044-579X
DOI	10.1016/j.semcancer.2022.07.005
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Article ; Online: Integration of Hybridization Strategies in Pyridine-Urea Scaffolds for Novel Anticancer Agents: Design, Synthesis, and Mechanistic Insights.

Godesi, Sreenivasulu / Nada, Hossam / Lee, Joohan / Kang, Joon-Hee / Kim, Soo-Youl / Choi, Yongseok / Lee, Kyeong

Molecules (Basel, Switzerland)

2023 Volume 28, Issue 13

Abstract: Annually, millions of new cancer cases are reported, leading to millions of deaths worldwide. Among the newly reported cases, breast and colon cancers prevail as the most frequently detected variations. To effectively counteract this rapid increase, the ... ...

Abstract	Annually, millions of new cancer cases are reported, leading to millions of deaths worldwide. Among the newly reported cases, breast and colon cancers prevail as the most frequently detected variations. To effectively counteract this rapid increase, the development of innovative therapies is crucial. Small molecules possessing pyridine and urea moieties have been reported in many of the currently available anticancer agents, especially VEGFR2 inhibitors. With this in mind, a rational design approach was employed to create hybrid small molecules combining urea and pyridine. These synthesized compounds underwent in vitro testing against breast and colon cancer cell lines, revealing potent submicromolar anticancer activity. Compound
MeSH term(s)	Humans ; Urea/pharmacology ; Structure-Activity Relationship ; Cell Line, Tumor ; Molecular Docking Simulation ; Antineoplastic Agents/pharmacology ; Pyridines/pharmacology ; Colonic Neoplasms ; Drug Screening Assays, Antitumor ; Cell Proliferation ; Molecular Structure
Chemical Substances	Urea (8W8T17847W) ; Antineoplastic Agents ; Pyridines
Language	English
Publishing date	2023-06-23
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	1413402-0
ISSN	1420-3049 ; 1431-5165 ; 1420-3049
ISSN (online)	1420-3049
ISSN	1431-5165 ; 1420-3049
DOI	10.3390/molecules28134952
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