Inhibition of the Nrf2-TrxR Axis Sensitizes the Drug-Resistant Chronic Myelogenous Leukemia Cell Line K562/G01 to Imatinib Treatments
Identifieur interne : 000724 ( Main/Exploration ); précédent : 000723; suivant : 000725Inhibition of the Nrf2-TrxR Axis Sensitizes the Drug-Resistant Chronic Myelogenous Leukemia Cell Line K562/G01 to Imatinib Treatments
Auteurs : Lianrong Xu [République populaire de Chine] ; Yan Zhao [République populaire de Chine] ; Fei Pan [République populaire de Chine] ; Mengxia Zhu [République populaire de Chine] ; Liqin Yao [République populaire de Chine] ; Yan Liu [République populaire de Chine] ; Jiangfang Feng [République populaire de Chine] ; Jie Xiong [République populaire de Chine] ; Xiuhua Chen [République populaire de Chine] ; Fanggang Ren [République populaire de Chine] ; Yanhong Tan [République populaire de Chine] ; Hongwei Wang [République populaire de Chine]Source :
- BioMed Research International [ 2314-6133 ] ; 2019.
Abstract
Nuclear factor erythroid 2-related factor 2 (Nrf2) is involved in tumor drug resistance, but its role in imatinib resistance of chronic myeloid leukemia (CML) remains elusive. We aimed to investigate the effects of Nrf2 on drug sensitivity, thioredoxin reductase (TrxR) expression, reactive oxygen species (ROS) production, and apoptosis induction in imatinib-resistant CML K562/G01 cells and explored their potential mechanisms. Stable K562/G01 cells with knockdown of Nrf2 were established by infection of siRNA-expressing lentivirus. The mRNA and protein expression levels of Nrf2 and TrxR were determined by real-time quantitative polymerase chain reaction and western blot, respectively. ROS generation and apoptosis were assayed by flow cytometry, while drug sensitivity was measured by the Cell Counting Kit-8 assay. Imatinib-resistant K562/G01 cells had higher levels of Nrf2 expression than the parental K562 cells at both mRNA and protein levels. Expression levels of Nrf2 and TrxR were positively correlated in K562/G01 cells. Knockdown of Nrf2 in K562/G01 cells enhanced the intracellular ROS level, suppressed cell proliferation, and increased apoptosis in response to imatinib treatments. Nrf2 expression contributes to the imatinib resistance of K562/G01 cells and is positively correlated with TrxR expression. Targeted inhibition of the Nrf2-TrxR axis represents a potential therapeutic approach for imatinib-resistant CML.
Url:
DOI: 10.1155/2019/6502793
PubMed: 31828114
PubMed Central: 6885806
Affiliations:
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sortKey="Xu, Lianrong" sort="Xu, Lianrong" uniqKey="Xu L" first="Lianrong" last="Xu">Lianrong Xu</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Hematology, 2nd Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Hematology, 2nd Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001</wicri:regionArea><wicri:noRegion>Shanxi 030001</wicri:noRegion></affiliation></author><author><name sortKey="Zhao, Yan" sort="Zhao, Yan" uniqKey="Zhao Y" first="Yan" last="Zhao">Yan Zhao</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Hematology, 2nd Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Hematology, 2nd Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001</wicri:regionArea><wicri:noRegion>Shanxi 030001</wicri:noRegion></affiliation></author><author><name sortKey="Pan, Fei" sort="Pan, Fei" uniqKey="Pan F" first="Fei" last="Pan">Fei Pan</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Hematology, 2nd Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Hematology, 2nd Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001</wicri:regionArea><wicri:noRegion>Shanxi 030001</wicri:noRegion></affiliation></author><author><name sortKey="Zhu, Mengxia" sort="Zhu, Mengxia" uniqKey="Zhu M" first="Mengxia" last="Zhu">Mengxia Zhu</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Hematology, 2nd Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Hematology, 2nd Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001</wicri:regionArea><wicri:noRegion>Shanxi 030001</wicri:noRegion></affiliation></author><author><name sortKey="Yao, Liqin" sort="Yao, Liqin" uniqKey="Yao L" first="Liqin" last="Yao">Liqin Yao</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Hematology, 2nd Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Hematology, 2nd Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001</wicri:regionArea><wicri:noRegion>Shanxi 030001</wicri:noRegion></affiliation></author><author><name sortKey="Liu, Yan" sort="Liu, Yan" uniqKey="Liu Y" first="Yan" last="Liu">Yan Liu</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Hematology, 2nd Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Hematology, 2nd Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001</wicri:regionArea><wicri:noRegion>Shanxi 030001</wicri:noRegion></affiliation></author><author><name sortKey="Feng, Jiangfang" sort="Feng, Jiangfang" uniqKey="Feng J" first="Jiangfang" last="Feng">Jiangfang Feng</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Hematology, 2nd Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Hematology, 2nd Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001</wicri:regionArea><wicri:noRegion>Shanxi 030001</wicri:noRegion></affiliation></author><author><name sortKey="Xiong, Jie" sort="Xiong, Jie" uniqKey="Xiong J" first="Jie" last="Xiong">Jie Xiong</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Hematology, 2nd Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Hematology, 2nd Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001</wicri:regionArea><wicri:noRegion>Shanxi 030001</wicri:noRegion></affiliation></author><author><name sortKey="Chen, Xiuhua" sort="Chen, Xiuhua" uniqKey="Chen X" first="Xiuhua" last="Chen">Xiuhua Chen</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Hematology, 2nd Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Hematology, 2nd Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001</wicri:regionArea><wicri:noRegion>Shanxi 030001</wicri:noRegion></affiliation></author><author><name sortKey="Ren, Fanggang" sort="Ren, Fanggang" uniqKey="Ren F" first="Fanggang" last="Ren">Fanggang Ren</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Hematology, 2nd Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Hematology, 2nd Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001</wicri:regionArea><wicri:noRegion>Shanxi 030001</wicri:noRegion></affiliation></author><author><name sortKey="Tan, Yanhong" sort="Tan, Yanhong" uniqKey="Tan Y" first="Yanhong" last="Tan">Yanhong Tan</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Hematology, 2nd Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Hematology, 2nd Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001</wicri:regionArea><wicri:noRegion>Shanxi 030001</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Hongwei" sort="Wang, Hongwei" uniqKey="Wang H" first="Hongwei" last="Wang">Hongwei Wang</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Hematology, 2nd Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Hematology, 2nd Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001</wicri:regionArea><wicri:noRegion>Shanxi 030001</wicri:noRegion></affiliation></author></analytic><series><title level="j">BioMed Research International</title><idno type="ISSN">2314-6133</idno><idno type="eISSN">2314-6141</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Nuclear factor erythroid 2-related factor 2 (Nrf2) is involved in tumor drug resistance, but its role in imatinib resistance of chronic myeloid leukemia (CML) remains elusive. We aimed to investigate the effects of Nrf2 on drug sensitivity, thioredoxin reductase (TrxR) expression, reactive oxygen species (ROS) production, and apoptosis induction in imatinib-resistant CML K562/G01 cells and explored their potential mechanisms. Stable K562/G01 cells with knockdown of Nrf2 were established by infection of siRNA-expressing lentivirus. The mRNA and protein expression levels of Nrf2 and TrxR were determined by real-time quantitative polymerase chain reaction and western blot, respectively. ROS generation and apoptosis were assayed by flow cytometry, while drug sensitivity was measured by the Cell Counting Kit-8 assay. Imatinib-resistant K562/G01 cells had higher levels of Nrf2 expression than the parental K562 cells at both mRNA and protein levels. Expression levels of Nrf2 and TrxR were positively correlated in K562/G01 cells. Knockdown of Nrf2 in K562/G01 cells enhanced the intracellular ROS level, suppressed cell proliferation, and increased apoptosis in response to imatinib treatments. Nrf2 expression contributes to the imatinib resistance of K562/G01 cells and is positively correlated with TrxR expression. Targeted inhibition of the Nrf2-TrxR axis represents a potential therapeutic approach for imatinib-resistant CML.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Flis, S" uniqKey="Flis S">S. Flis</name></author><author><name sortKey="Chojnacki, T" uniqKey="Chojnacki T">T. Chojnacki</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Stagno, F" uniqKey="Stagno F">F. Stagno</name></author><author><name sortKey="Stella, S" uniqKey="Stella S">S. Stella</name></author><author><name sortKey="Spitaleri, A" uniqKey="Spitaleri A">A. Spitaleri</name></author><author><name sortKey="Pennisi, M S" uniqKey="Pennisi M">M. S. 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