Luteolin suppresses cancer cell proliferation by targeting vaccinia-related kinase 1

Uncontrolled proliferation, a major feature of cancer cells, is often triggered by the malfunction of cell cycle regulators such as protein kinases. Recently, cell cycle-related protein kinases have become attractive targets for anti-cancer therapy, because they play fundamental roles in cellular pr...

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Published inPloS one Vol. 9; no. 10; p. e109655
Main Authors Kim, Ye Seul, Kim, Seong-Hoon, Shin, Joon, Harikishore, Amaravadhi, Lim, Jong-Kwan, Jung, Youngseob, Lyu, Ha-Na, Baek, Nam-In, Choi, Kwan Yong, Yoon, Ho Sup, Kim, Kyong-Tai
Format Journal Article
LanguageEnglish
Published United States Public Library of Science 13.10.2014
Public Library of Science (PLoS)
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Abstract Uncontrolled proliferation, a major feature of cancer cells, is often triggered by the malfunction of cell cycle regulators such as protein kinases. Recently, cell cycle-related protein kinases have become attractive targets for anti-cancer therapy, because they play fundamental roles in cellular proliferation. However, the protein kinase-targeted drugs that have been developed so far do not show impressive clinical results and also display severe side effects; therefore, there is undoubtedly a need to investigate new drugs targeting other protein kinases that are critical in cell cycle progression. Vaccinia-related kinase 1 (VRK1) is a mitotic kinase that functions in cell cycle regulation by phosphorylating cell cycle-related substrates such as barrier-to-autointegration factor (BAF), histone H3, and the cAMP response element (CRE)-binding protein (CREB). In our study, we identified luteolin as the inhibitor of VRK1 by screening a small-molecule natural compound library. Here, we evaluated the efficacy of luteolin as a VRK1-targeted inhibitor for developing an effective anti-cancer strategy. We confirmed that luteolin significantly reduces VRK1-mediated phosphorylation of the cell cycle-related substrates BAF and histone H3, and directly interacts with the catalytic domain of VRK1. In addition, luteolin regulates cell cycle progression by modulating VRK1 activity, leading to the suppression of cancer cell proliferation and the induction of apoptosis. Therefore, our study suggests that luteolin-induced VRK1 inhibition may contribute to establish a novel cell cycle-targeted strategy for anti-cancer therapy.
AbstractList Uncontrolled proliferation, a major feature of cancer cells, is often triggered by the malfunction of cell cycle regulators such as protein kinases. Recently, cell cycle-related protein kinases have become attractive targets for anti-cancer therapy, because they play fundamental roles in cellular proliferation. However, the protein kinase-targeted drugs that have been developed so far do not show impressive clinical results and also display severe side effects; therefore, there is undoubtedly a need to investigate new drugs targeting other protein kinases that are critical in cell cycle progression. Vaccinia-related kinase 1 (VRK1) is a mitotic kinase that functions in cell cycle regulation by phosphorylating cell cycle-related substrates such as barrier-to-autointegration factor (BAF), histone H3, and the cAMP response element (CRE)-binding protein (CREB). In our study, we identified luteolin as the inhibitor of VRK1 by screening a small-molecule natural compound library. Here, we evaluated the efficacy of luteolin as a VRK1-targeted inhibitor for developing an effective anti-cancer strategy. We confirmed that luteolin significantly reduces VRK1-mediated phosphorylation of the cell cycle-related substrates BAF and histone H3, and directly interacts with the catalytic domain of VRK1. In addition, luteolin regulates cell cycle progression by modulating VRK1 activity, leading to the suppression of cancer cell proliferation and the induction of apoptosis. Therefore, our study suggests that luteolin-induced VRK1 inhibition may contribute to establish a novel cell cycle-targeted strategy for anti-cancer therapy.
Audience Academic
Author Yoon, Ho Sup
Shin, Joon
Choi, Kwan Yong
Kim, Seong-Hoon
Baek, Nam-In
Lim, Jong-Kwan
Kim, Kyong-Tai
Lyu, Ha-Na
Harikishore, Amaravadhi
Jung, Youngseob
Kim, Ye Seul
AuthorAffiliation 1 Department of Life Sciences, Pohang University of Science and Technology, Pohang, Republic of Korea
2 School of Biological Sciences, Nanyang Technological University, Singapore, Singapore
4 The Graduate School of Biotechnology and Plant Metabolism Research Center, Kyung-Hee University, Suwon, Republic of Korea
3 Division of Integrative Biosciences and Biotechnology, Pohang University of Science and Technology, Pohang, Republic of Korea
Winship Cancer Institute of Emory University, United States of America
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/25310002$$D View this record in MEDLINE/PubMed
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2014 Kim et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
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– notice: 2014 Kim et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
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Conceived and designed the experiments: YSK SHK KYC KTK. Performed the experiments: YSK SHK JS AH HNL JKL YSJ. Analyzed the data: YSK JS AH HSY KTK. Contributed reagents/materials/analysis tools: NIB. Wrote the paper: YSK SHK JS HSY KTK.
Competing Interests: The authors have declared that no competing interests exist.
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SSID ssj0053866
Score 2.3709986
Snippet Uncontrolled proliferation, a major feature of cancer cells, is often triggered by the malfunction of cell cycle regulators such as protein kinases. Recently,...
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SourceType Open Website
Open Access Repository
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StartPage e109655
SubjectTerms Anticancer properties
Antineoplastic Agents - chemistry
Antineoplastic Agents - pharmacology
Apoptosis
B cells
Biology and Life Sciences
Biotechnology
Cancer
Cancer therapies
Catalysis
Catalytic Domain - drug effects
Cell cycle
Cell division
Cell growth
Cell Line, Tumor
Cell proliferation
Cell Proliferation - drug effects
Cyclic AMP response element-binding protein
Deoxyribonucleic acid
DNA
DNA damage
DNA-Binding Proteins - metabolism
Drug delivery
Drugs
Flavonoids
Health aspects
Histone H3
Histones - metabolism
Humans
Inhibitors
Intracellular Signaling Peptides and Proteins - antagonists & inhibitors
Intracellular Signaling Peptides and Proteins - chemistry
Kinases
Life sciences
Luteolin - chemistry
Luteolin - pharmacology
Metastasis
Nuclear Proteins - metabolism
Phase transitions
Phosphatase
Phosphorylation
Phosphorylation - drug effects
Phosphotransferases
Polyphenols
Protein binding
Protein kinase
Protein-Serine-Threonine Kinases - antagonists & inhibitors
Protein-Serine-Threonine Kinases - chemistry
Proteins
Regulators
Side effects
Substrates
Therapy
Vaccinia
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Title Luteolin suppresses cancer cell proliferation by targeting vaccinia-related kinase 1
URI https://www.ncbi.nlm.nih.gov/pubmed/25310002
https://www.proquest.com/docview/1610992832
https://search.proquest.com/docview/1612290356
https://pubmed.ncbi.nlm.nih.gov/PMC4195671
https://doaj.org/article/c3ea2e19b3704363a0252fb2173d9e37
http://dx.doi.org/10.1371/journal.pone.0109655
Volume 9
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