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Biomolecules and Their Impact on Biology and Translational Applications: Celebrating...
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Biomolecules and Their Impact on Biology and Translational Applications: Celebrating the Pioneering Work of Prof. Ho Jeong Kwon

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Cellular Biochemistry".

Deadline for manuscript submissions: closed (31 December 2024) | Viewed by 14457

Special Issue Editors

Dr. Eun-Woo Lee

E-Mail Website
Guest Editor
Metabolic Regulation Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon 34141, Republic of Korea
Interests: ferroptosis; lipid metabolism; cancer metabolism; cardiovascular diseases; drug development
Special Issues, Collections and Topics in MDPI journals
Dr. Hye Jin Kang

E-Mail Website
Guest Editor
Department of Biotechnology, College of Life Science and Biotechnology, Yonsei University, Seoul, Republic of Korea
Interests: GPCR pharmacology; chemogenetics; tool compounds; pain and itch

Special Issue Information

Dear Colleagues,

This year marks the 25th anniversary of the publication of Professor Ho Jeong Kwon’s paper (PNAS, 95:3356, 1998), in which he reported a new inventory of biological tools using “depudecin’ as a pharmacologically active compound for the study of, and for medical intervention in, basic biological processes. This paper stimulated the interest of many researchers and physicians to explore the biological role of histone deacetylases in gene regulation.

The addition of depudecin to pharmacopoeia has the potential to contribute to both basic and clinical science; for instance, its novel structure has already contributed to the understanding of the enzymatic mechanisms of action of the deacetylases, and it may further have unique advantages for therapeutic purposes. The past 25 years have witnessed intense scientific efforts to discover new biomolecules for advancing biology and biomedical applications. Professor Kwon has been at the forefront of these innovative efforts, conducting pioneering research on some of the angiogenesis- and autophagy-regulating biomolecules such as terpestacin, curcumin, kaempferide, Rg3, sertraline, artemisinate, daptomycin, voacangine, crytotashinone, etc., as well as on the biological roles of the targets of these biomolecules and their translational applications in health and disease, providing insights into the “biomolecule-target-phenotype’ link in biology and translational applications.

This Special Issue aims to focus on the role of biomolecules and their impact on biology and translational applications. It will begin with a brief review of Professor Kwon’s contributions to this field, followed by original research articles and reviews on all aspects of the molecular mechanisms and functional actions of biomolecules and their applications in health and disease.

Dr. Eun-Woo Lee
Dr. Hye Jin Kang
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • biomolecules
  • cancer
  • angiogenesis
  • autophagy
  • GPCRs
  • translational applications
  • target identification
  • proximity-labeling
  • molecular docking
  • molecular probe
  • molecular pharmacology

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Published Papers (10 papers)

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Research

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15 pages, 2950 KiB  
Article
Involvement of RhoA/ROCK Signaling Pathway in Methamphetamine-Induced Blood-Brain Barrier Disruption
by Jong Su Hwang, Tam Thuy Lu Vo, Mikyung Kim, Eun Hye Cha, Kyo Cheol Mun, Eunyoung Ha and Ji Hae Seo
Biomolecules 2025, 15(3), 340; https://doi.org/10.3390/biom15030340 - 27 Feb 2025
Viewed by 577
Abstract
Methamphetamine (METH) is a powerful addictive psychostimulant that gives rise to severe abusers worldwide. While many studies have reported on the neurotoxicity of METH, blood–brain barrier (BBB) dysfunction has recently attracted attention as an essential target in METH-induced pathological changes in the brain. [...] Read more.
Methamphetamine (METH) is a powerful addictive psychostimulant that gives rise to severe abusers worldwide. While many studies have reported on the neurotoxicity of METH, blood–brain barrier (BBB) dysfunction has recently attracted attention as an essential target in METH-induced pathological changes in the brain. However, its mechanism has not been fully understood. We found that METH increased paracellular permeability and decreased vascular integrity through FITC–dextran and trans-endothelial electrical resistance (TEER) assay in primary human brain endothelial cells (HBMECs). Also, redistribution of tight junction proteins (zonula occluden-1 and claudin-5) and reorganization of F-actin cytoskeleton were observed in METH-exposed HBMECs. To determine the mechanism of METH-induced BBB disruption, the RhoA/ROCK signaling pathway was examined in METH-treated HBMECs. METH-activated RhoA, followed by an increase in the phosphorylation of downstream effectors, myosin light chain (MLC) and cofilin, occurs in HBMECs. Pretreatment with ROCK inhibitors Y-27632 and fasudil reduced the METH-induced increase in phosphorylation of MLC and cofilin, preventing METH-induced redistribution of junction proteins and F-actin cytoskeletal reorganization. Moreover, METH-induced BBB leakage was alleviated by ROCK inhibitors in vitro and in vivo. Taken together, these results suggest that METH induces BBB dysfunction by activating the RhoA/ROCK signaling pathway, which results in the redistribution of junction proteins via F-actin cytoskeletal reorganization. Full article
(This article belongs to the Special Issue Biomolecules and Their Impact on Biology and Translational Applications: Celebrating the Pioneering Work of Prof. Ho Jeong Kwon)
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14 pages, 4934 KiB  
Article
TRPC6-Mediated Zn2+ Influx Negatively Regulates Contractile Differentiation of Vascular Smooth Muscle Cells
by Chenlin Su, Xinya Mi, Tomoya Ito, Yuri Kato, Akiyuki Nishimura, Ryu Nagata, Yasuo Mori and Motohiro Nishida
Biomolecules 2025, 15(2), 267; https://doi.org/10.3390/biom15020267 - 12 Feb 2025
Viewed by 672
Abstract
Vascular smooth muscle cells (VSMCs) can dynamically change their phenotype between contractile and synthetic forms in response to environmental stress, which is pivotal in maintaining vascular homeostasis and mediating pathological remodeling of blood vessels. We previously reported that suppression of canonical transient receptor [...] Read more.
Vascular smooth muscle cells (VSMCs) can dynamically change their phenotype between contractile and synthetic forms in response to environmental stress, which is pivotal in maintaining vascular homeostasis and mediating pathological remodeling of blood vessels. We previously reported that suppression of canonical transient receptor potential 6 (TRPC6) channel-mediated cation entry sustains VSMCs contractile phenotype and promotes the blood flow recovery after hindlimb ischemia in mice. We also reported that Zn2+, a metal biomolecule mobilized by TRPC6 channel activation, exerts potential beneficial effects on cardiac contractility and remodeling. Therefore, we hypothesized that TRPC6-mediated Zn2+ influx participates in phenotype switching of VSMCs and vascular remodeling. We established rat aortic smooth muscle cells (RAoSMCs) stably expressing wild type (WT) and Zn2+ only impermeable TRPC6 (KYD) mutant. Although the resting phenotypes were similar in both RAoSMCs, pharmacological TRPC6 activation by PPZ2 prevented the transforming growth factor (TGF) β-induced reduction in the intracellular Zn2+ amount and contractile differentiation in RAoSMCs (WT), but failed to prevent them in RAoSMCs (KYD). There were no significant differences in TRPC6-dependent cation currents among all RAoSMCs pretreated with or without TGFβ and/or PPZ2, suggesting that TRPC6 channels are functionally expressed in RAoSMCs regardless of their phenotype. Treatment of mice with PPZ2 attenuated the progression of vascular remodeling caused by chronic angiotensin II infusion. These results suggest that Zn2+ influx through TRPC6 channels negatively regulates the TGFβ-induced contractile differentiation of VSMCs and the progression of vascular remodeling in rodents. Full article
(This article belongs to the Special Issue Biomolecules and Their Impact on Biology and Translational Applications: Celebrating the Pioneering Work of Prof. Ho Jeong Kwon)
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16 pages, 7466 KiB  
Article
Urolithin A Protects Hepatocytes from Palmitic Acid-Induced ER Stress by Regulating Calcium Homeostasis in the MAM
by Gayoung Ryu, Minjeong Ko, Sooyeon Lee, Se In Park, Jin-Woong Choi, Ju Yeon Lee, Jin Young Kim and Ho Jeong Kwon
Biomolecules 2024, 14(12), 1505; https://doi.org/10.3390/biom14121505 - 26 Nov 2024
Viewed by 1326
Abstract
An ellagitannin-derived metabolite, Urolithin A (UA), has emerged as a potential therapeutic agent for metabolic disorders due to its antioxidant, anti-inflammatory, and mitochondrial function-improving properties, but its efficacy in protecting against ER stress remains underexplored. The endoplasmic reticulum (ER) is a cellular organelle [...] Read more.
An ellagitannin-derived metabolite, Urolithin A (UA), has emerged as a potential therapeutic agent for metabolic disorders due to its antioxidant, anti-inflammatory, and mitochondrial function-improving properties, but its efficacy in protecting against ER stress remains underexplored. The endoplasmic reticulum (ER) is a cellular organelle involved in protein folding, lipid synthesis, and calcium regulation. Perturbations in these functions can lead to ER stress, which contributes to the development and progression of metabolic disorders such as metabolic-associated fatty liver disease (MAFLD). In this study, we identified a novel target protein of UA and elucidated its mechanism for alleviating palmitic acid (PA)-induced ER stress. Cellular thermal shift assay (CETSA)-LC-MS/MS analysis revealed that UA binds directly to the sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA), an important regulator of calcium homeostasis in mitochondria-associated ER membranes (MAMs). As an agonist of SERCA, UA attenuates abnormal calcium fluctuations and ER stress in PA-treated liver cells, thereby contributing to cell survival. The lack of UA activity in SERCA knockdown cells suggests that UA regulates cellular homeostasis through its interaction with SERCA. Collectively, our results demonstrate that UA protects against PA-induced ER stress and enhances cell survival by regulating calcium homeostasis in MAMs through SERCA. This study highlights the potential of UA as a therapeutic agent for metabolic disorders associated with ER stress. Full article
(This article belongs to the Special Issue Biomolecules and Their Impact on Biology and Translational Applications: Celebrating the Pioneering Work of Prof. Ho Jeong Kwon)
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15 pages, 4488 KiB  
Article
IFN-γ-Preconditioned Human Gingival-Derived Mesenchymal Stromal Cells Inhibit Plasmacytoid Dendritic Cells via Adenosine
by William de Jesús Ríos-Ríos, Sorely Adelina Sosa-Luis, Alexia Almaraz-Arreortua, Patricia Vargas-Benitez, Héctor Ulises Bernardino-Hernández, Jaime Vargas-Arzola, Luis Alberto Hernández-Osorio, María de los Ángeles Romero-Tlalolini, Sergio Roberto Aguilar-Ruiz and Honorio Torres-Aguilar
Biomolecules 2024, 14(6), 658; https://doi.org/10.3390/biom14060658 - 4 Jun 2024
Viewed by 1587
Abstract
Plasmacytoid dendritic cells (pDCs) are vital players in antiviral immune responses because of their high levels of IFN-α secretion. However, this attribute has also implicated them as critical factors behind the immunopathogenesis of inflammatory diseases, and no currently available therapy can efficiently inhibit [...] Read more.
Plasmacytoid dendritic cells (pDCs) are vital players in antiviral immune responses because of their high levels of IFN-α secretion. However, this attribute has also implicated them as critical factors behind the immunopathogenesis of inflammatory diseases, and no currently available therapy can efficiently inhibit pDCs’ aberrant activation. Mesenchymal stromal cells (MSCs) possess stromal immunomodulatory functionality, regulating immune cell activation through several mechanisms, including the adenosinergic (CD39/CD73/adenosine) pathway. The IFN-γ preconditioning of bone marrow MSCs improves their inhibitory properties for therapy applications; however, isolating human gingival tissue-derived MSCs (hGMSCs) is more accessible. These cells have shown better immunomodulatory effects, yet the outcome of IFN-γ preconditioning and its impact on the adenosinergic pathway has not been evaluated. This study first validated the immunoregulatory properties of primary-cultured hGMSCs, and the results showed that IFN-γ preconditioning strengthens CD39/CD73 coexpression, adenosine production, and the regulatory properties of hGMSC, which were confirmed by describing for the first time their ability to reduce pDC activation and their IFN-α secretion and to increase the frequency of CD73+ pDC. In addition, when CD73′s enzymatic activity was neutralized in hGMSCs, adenosine production and the IFN-γ preconditioning effect were restrained. This evidence might be applied to design hGMSCs- and adenosine-based immunotherapeutic strategies for treating inflammatory disorders that are associated with pDC overactivation. Full article
(This article belongs to the Special Issue Biomolecules and Their Impact on Biology and Translational Applications: Celebrating the Pioneering Work of Prof. Ho Jeong Kwon)
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21 pages, 5374 KiB  
Article
Lysophosphatidic Acid Stimulates Mitogenic Activity and Signaling in Human Neuroblastoma Cells through a Crosstalk with Anaplastic Lymphoma Kinase
by Simona Dedoni, Maria C. Olianas and Pierluigi Onali
Biomolecules 2024, 14(6), 631; https://doi.org/10.3390/biom14060631 - 28 May 2024
Cited by 1 | Viewed by 1654
Abstract
Lysophosphatidic acid (LPA) is a well-documented pro-oncogenic factor in different cancers, but relatively little is known on its biological activity in neuroblastoma. The LPA effects and the participation of the tyrosine kinase receptor anaplastic lymphoma kinase (ALK) in LPA mitogenic signaling were studied [...] Read more.
Lysophosphatidic acid (LPA) is a well-documented pro-oncogenic factor in different cancers, but relatively little is known on its biological activity in neuroblastoma. The LPA effects and the participation of the tyrosine kinase receptor anaplastic lymphoma kinase (ALK) in LPA mitogenic signaling were studied in human neuroblastoma cell lines. We used light microscopy and [3H]-thymidine incorporation to determine cell proliferation, Western blot to study intracellular signaling, and pharmacological and molecular tools to examine the role of ALK. We found that LPA stimulated the growth of human neuroblastoma cells, as indicated by the enhanced cell number, clonogenic activity, and DNA synthesis. These effects were curtailed by the selective ALK inhibitors NPV-TAE684 and alectinib. In a panel of human neuroblastoma cell lines harboring different ALK genomic status, the ALK inhibitors suppressed LPA-induced phosphorylation of extracellular signal-regulated kinases 1/2 (ERK1/2), which are major regulators of cell proliferation. ALK depletion by siRNA treatment attenuated LPA-induced ERK1/2 activation. LPA enhanced ALK phosphorylation and potentiated ALK activation by the ALK ligand FAM150B. LPA enhanced the inhibitory phosphorylation of the tumor suppressor FoxO3a, and this response was impaired by the ALK inhibitors. These results indicate that LPA stimulates mitogenesis of human neuroblastoma cells through a crosstalk with ALK. Full article
(This article belongs to the Special Issue Biomolecules and Their Impact on Biology and Translational Applications: Celebrating the Pioneering Work of Prof. Ho Jeong Kwon)
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22 pages, 6558 KiB  
Article
Unlocking Potential: Low Bovine Serum Albumin Enhances the Chondrogenicity of Human Adipose-Derived Stromal Cells in Pellet Cultures
by Isabel Casado-Losada, Melanie Acosta, Barbara Schädl, Eleni Priglinger, Susanne Wolbank and Sylvia Nürnberger
Biomolecules 2024, 14(4), 413; https://doi.org/10.3390/biom14040413 - 28 Mar 2024
Viewed by 1707
Abstract
Bovine serum albumin (BSA) plays a crucial role in cell culture media, influencing cellular processes such as proliferation and differentiation. Although it is commonly included in chondrogenic differentiation media, its specific function remains unclear. This study explores the effect of different BSA concentrations [...] Read more.
Bovine serum albumin (BSA) plays a crucial role in cell culture media, influencing cellular processes such as proliferation and differentiation. Although it is commonly included in chondrogenic differentiation media, its specific function remains unclear. This study explores the effect of different BSA concentrations on the chondrogenic differentiation of human adipose-derived stromal/stem cells (hASCs). hASC pellets from six donors were cultured under chondrogenic conditions with three BSA concentrations. Surprisingly, a lower BSA concentration led to enhanced chondrogenesis. The degree of this effect was donor-dependent, classifying them into two groups: (1) high responders, forming at least 35% larger, differentiated pellets with low BSA in comparison to high BSA; (2) low responders, which benefitted only slightly from low BSA doses with a decrease in pellet size and marginal differentiation, indicative of low intrinsic differentiation potential. In all cases, increased chondrogenesis was accompanied by hypertrophy under low BSA concentrations. To the best of our knowledge, this is the first study showing improved chondrogenicity and the tendency for hypertrophy with low BSA concentration compared to standard levels. Once the tendency for hypertrophy is understood, the determination of BSA concentration might be used to tune hASC chondrogenic or osteogenic differentiation. Full article
(This article belongs to the Special Issue Biomolecules and Their Impact on Biology and Translational Applications: Celebrating the Pioneering Work of Prof. Ho Jeong Kwon)
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Review

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13 pages, 2123 KiB  
Review
Quercetin: Molecular Insights into Its Biological Roles
by Hye Joon Boo, Danbi Yoon, Yujeong Choi, Younghyun Kim, Jeong Seok Cha and Jiho Yoo
Biomolecules 2025, 15(3), 313; https://doi.org/10.3390/biom15030313 - 20 Feb 2025
Viewed by 616
Abstract
Quercetin, a prevalent plant flavonoid, demonstrates many biological functions through its interaction with distinct protein targets. Recent structural investigations of protein–quercetin complexes have elucidated the molecular mechanism behind these actions. This paper presents a thorough structural analysis of experimentally established protein–quercetin complex structures [...] Read more.
Quercetin, a prevalent plant flavonoid, demonstrates many biological functions through its interaction with distinct protein targets. Recent structural investigations of protein–quercetin complexes have elucidated the molecular mechanism behind these actions. This paper presents a thorough structural analysis of experimentally established protein–quercetin complex structures published to date. The structure of the protein–quercetin complex elucidates the molecular mechanism by which quercetin influences protein function. These structures illustrate how quercetin’s chemical characteristics facilitate diverse modes of action by enabling particular interactions with the target protein. This structural knowledge provides the molecular foundation for comprehending quercetin’s biological roles and indicates avenues for future structural investigations of flavonoid–protein complexes, especially those with ambiguous molecular processes. Full article
(This article belongs to the Special Issue Biomolecules and Their Impact on Biology and Translational Applications: Celebrating the Pioneering Work of Prof. Ho Jeong Kwon)
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25 pages, 6918 KiB  
Review
G-Protein-Coupled Receptor (GPCR) Signaling and Pharmacology in Metabolism: Physiology, Mechanisms, and Therapeutic Potential
by Yun Yeong Cho, Soyeon Kim, Pankyung Kim, Min Jeong Jo, Song-E Park, Yiju Choi, Su Myung Jung and Hye Jin Kang
Biomolecules 2025, 15(2), 291; https://doi.org/10.3390/biom15020291 - 15 Feb 2025
Cited by 1 | Viewed by 1952
Abstract
G-protein coupled receptors (GPCRs), the largest family of integral membrane proteins, enable cells to sense and appropriately respond to the environment through mediating extracellular signaling to intercellular messenger molecules. GPCRs’ pairing with a diverse array of G protein subunits and related downstream secondary [...] Read more.
G-protein coupled receptors (GPCRs), the largest family of integral membrane proteins, enable cells to sense and appropriately respond to the environment through mediating extracellular signaling to intercellular messenger molecules. GPCRs’ pairing with a diverse array of G protein subunits and related downstream secondary messengers, combined with their ligand versatility-from conventional peptide hormone to numerous bioactive metabolites, allow GPCRs to comprehensively regulate metabolism and physiology. Consequently, GPCRs have garnered significant attention for their therapeutic potential in metabolic diseases. This review focuses on six GPCRs, GPR40, GPR120, GLP-1R, and ß-adrenergic receptors (ADRB1, ADRB2, and ADRB3), with GLP-1R recognized as a prominent regulator of system-level metabolism, while the roles of GPR40, GPR120 and ß-adrenergic receptors in central carbon metabolism and energy homeostasis are increasingly appreciated. Here, we discuss their physiological functions in metabolism, the current pharmacological landscape, and the intricacies of their signaling pathways via G protein and ß-arrestin activation. Additionally, we discuss the limitations of existing GPCR-targeted strategies for treating metabolic diseases and offer insights into future perspectives for advancing GPCR pharmacology. Full article
(This article belongs to the Special Issue Biomolecules and Their Impact on Biology and Translational Applications: Celebrating the Pioneering Work of Prof. Ho Jeong Kwon)
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15 pages, 5854 KiB  
Review
Exploring the Antiangiogenic and Anti-Inflammatory Potential of Homoisoflavonoids: Target Identification Using Biotin Probes
by Xiang Fei, Sangil Kwon, Jinyoung Jang, Minyoung Seo, Seongwon Yu, Timothy W. Corson and Seung-Yong Seo
Biomolecules 2024, 14(7), 785; https://doi.org/10.3390/biom14070785 - 30 Jun 2024
Cited by 1 | Viewed by 1857
Abstract
Chemical proteomics using biotin probes of natural products have significantly advanced our understanding of molecular targets and therapeutic potential. This review highlights recent progress in the application of biotin probes of homoisoflavonoids for identifying binding proteins and elucidating mechanisms of action. Notably, homoisoflavonoids [...] Read more.
Chemical proteomics using biotin probes of natural products have significantly advanced our understanding of molecular targets and therapeutic potential. This review highlights recent progress in the application of biotin probes of homoisoflavonoids for identifying binding proteins and elucidating mechanisms of action. Notably, homoisoflavonoids exhibit antiangiogenic, anti-inflammatory, and antidiabetic effects. A combination of biotin probes, pull-down assays, mass spectrometry, and molecular modeling has revealed how natural products and their derivatives interact with several proteins such as ferrochelatase (FECH), soluble epoxide hydrolase (sEH), inosine monophosphate dehydrogenase 2 (IMPDH2), phosphodiesterase 4 (PDE4), and deoxyhypusine hydroxylase (DOHH). These target identification approaches pave the way for new therapeutic avenues, especially in the fields of oncology and ophthalmology. Future research aimed at expanding the repertoire of target identification using biotin probes of homoisoflavonoids promises to further elucidate the complex mechanisms and develop new drug candidates. Full article
(This article belongs to the Special Issue Biomolecules and Their Impact on Biology and Translational Applications: Celebrating the Pioneering Work of Prof. Ho Jeong Kwon)
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Other

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12 pages, 2297 KiB  
Brief Report
Enhanced Anticancer Activity of 7MeERT over Ertredin: A Comparative Study on Cancer Cell Proliferation and NDUFA12 Binding
by Sonoko Atsumi, Chisato Nosaka, Takefumi Onodera, Hayamitsu Adachi, Takumi Watanabe, Manabu Kawada, Masabumi Shibuya, Se In Park and Ho Jeong Kwon
Biomolecules 2024, 14(9), 1197; https://doi.org/10.3390/biom14091197 - 23 Sep 2024
Viewed by 1199
Abstract
We have previously identified Ertredin (3-(2-amino-5-bromophenyl) quinoxalin-2(1H)-one) as a compound that suppresses 3D spheroid formation and tumorigenesis in NIH3T3 cells induced by Epidermal Growth Factor Receptor variant III (EGFRvIII) transduction. One of its targets has been shown to be NDUFA12 (NADH [...] Read more.
We have previously identified Ertredin (3-(2-amino-5-bromophenyl) quinoxalin-2(1H)-one) as a compound that suppresses 3D spheroid formation and tumorigenesis in NIH3T3 cells induced by Epidermal Growth Factor Receptor variant III (EGFRvIII) transduction. One of its targets has been shown to be NDUFA12 (NADH Dehydrogenase (Ubiquinone) 1 Alpha Subcomplex Subunit 12), a component protein of oxidative phosphorylation complex I. In this report, we compared the growth inhibitory activity of Ertredin with its methylated analogue 7MeERT (3-(2-amino-5-bromophenyl)-7-methylquinoxalin-2(1H)-one) on human cancer cells. 7MeERT induced the inhibition of the proliferation of various cancer cells similarly to Ertredin and showed higher activity in glioblastoma cells, A431 cells overexpressing EGFR (wild type), and multiple myeloma cells. Molecular docking analysis and a Cellular Thermal Shift Assay (CETSA) suggested that 7MeERT binds to NDUFA12 similarly to Ertredin. The binding of 7MeERT and Ertredin to NDUFA12 in glioblastoma was further supported by the inhibition of the oxygen consumption rate. These results suggest that 7MeERT also binds to NDUFA12, inhibits oxidative phosphorylation, and has a higher anti-cancer cell growth inhibitory activity than Ertredin. Full article
(This article belongs to the Special Issue Biomolecules and Their Impact on Biology and Translational Applications: Celebrating the Pioneering Work of Prof. Ho Jeong Kwon)
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