Quinacrine-Mediated Inhibition of Nrf2 Reverses Hypoxia-Induced 5-Fluorouracil Resistance in Colorectal Cancer
Identifieur interne : 000495 ( Main/Exploration ); précédent : 000494; suivant : 000496Quinacrine-Mediated Inhibition of Nrf2 Reverses Hypoxia-Induced 5-Fluorouracil Resistance in Colorectal Cancer
Auteurs : Ha Gyeong Kim ; Chan Woo Kim ; Don Haeng Lee [Corée du Sud] ; Jae-Seon Lee [Corée du Sud] ; Eun-Taex Oh [Corée du Sud] ; Heon Joo Park [Corée du Sud]Source :
- International Journal of Molecular Sciences [ 1422-0067 ] ; 2019.
Abstract
5-Fluorouracil (5-FU) is an important chemotherapeutic agent for the systemic treatment of colorectal cancer (CRC), but its effectiveness against CRC is limited by increased 5-FU resistance caused by the hypoxic tumor microenvironment. The purpose of our study was to assess the feasibility of using quinacrine (QC) to increase the efficacy of 5-FU against CRC cells under hypoxic conditions. QC reversed the resistance to 5-FU induced by hypoxia in CRC cell lines, as determined using ATP-Glo cell viability assays and clonogenic survival assays. Treatment of cells with 5-FU under hypoxic conditions had no effect on the expression of nuclear factor (erythroid-derived 2)-like 2 (Nrf2), a regulator of cellular resistance to oxidative stress, whereas treatment with QC alone or in combination with 5-FU reduced Nrf2 expression in all CRC cell lines tested. Overexpression of Nrf2 effectively prevented the increase in the number of DNA double-strand breaks induced by QC alone or in combination with 5-FU. siRNA-mediated c-Jun
Url:
DOI: 10.3390/ijms20184366
PubMed: 31491980
PubMed Central: 6770959
Affiliations:
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(C.W.K.)</nlm:aff><wicri:noCountry code="subfield">Korea (H.G.K.) (C.W.K.)</wicri:noCountry></affiliation></author><author><name sortKey="Kim, Chan Woo" sort="Kim, Chan Woo" uniqKey="Kim C" first="Chan Woo" last="Kim">Chan Woo Kim</name><affiliation><nlm:aff id="af1-ijms-20-04366">Department of Microbiology, College of Medicine, Inha University, Incheon 22212, Korea (H.G.K.) (C.W.K.)</nlm:aff><wicri:noCountry code="subfield">Korea (H.G.K.) (C.W.K.)</wicri:noCountry></affiliation></author><author><name sortKey="Lee, Don Haeng" sort="Lee, Don Haeng" uniqKey="Lee D" first="Don Haeng" last="Lee">Don Haeng Lee</name><affiliation wicri:level="1"><nlm:aff id="af2-ijms-20-04366">Department of Internal Medicine, College of Medicine, Inha University, Incheon 22212, Korea</nlm:aff><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Internal Medicine, College of Medicine, Inha University, Incheon 22212</wicri:regionArea><wicri:noRegion>Incheon 22212</wicri:noRegion></affiliation></author><author><name sortKey="Lee, Jae Seon" sort="Lee, Jae Seon" uniqKey="Lee J" first="Jae-Seon" last="Lee">Jae-Seon Lee</name><affiliation wicri:level="1"><nlm:aff id="af3-ijms-20-04366">Department of Molecular Medicine, College of Medicine, Inha University, Incheon 22212, Korea</nlm:aff><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Molecular Medicine, College of Medicine, Inha University, Incheon 22212</wicri:regionArea><wicri:noRegion>Incheon 22212</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="af4-ijms-20-04366">Hypoxia-related Disease Research Center, College of Medicine, Inha University, Incheon 22212, Korea</nlm:aff><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Hypoxia-related Disease Research Center, College of Medicine, Inha University, Incheon 22212</wicri:regionArea><wicri:noRegion>Incheon 22212</wicri:noRegion></affiliation></author><author><name sortKey="Oh, Eun Taex" sort="Oh, Eun Taex" uniqKey="Oh E" first="Eun-Taex" last="Oh">Eun-Taex Oh</name><affiliation wicri:level="1"><nlm:aff id="af4-ijms-20-04366">Hypoxia-related Disease Research Center, College of Medicine, Inha University, Incheon 22212, Korea</nlm:aff><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Hypoxia-related Disease Research Center, College of Medicine, Inha University, Incheon 22212</wicri:regionArea><wicri:noRegion>Incheon 22212</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="af5-ijms-20-04366">Department of Biomedical Sciences, College of Medicine, Inha University, Incheon 22212, Korea</nlm:aff><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Biomedical Sciences, College of Medicine, Inha University, Incheon 22212</wicri:regionArea><wicri:noRegion>Incheon 22212</wicri:noRegion></affiliation></author><author><name sortKey="Park, Heon Joo" sort="Park, Heon Joo" uniqKey="Park H" first="Heon Joo" last="Park">Heon Joo Park</name><affiliation><nlm:aff id="af1-ijms-20-04366">Department of Microbiology, College of Medicine, Inha University, Incheon 22212, Korea (H.G.K.) (C.W.K.)</nlm:aff><wicri:noCountry code="subfield">Korea (H.G.K.) (C.W.K.)</wicri:noCountry></affiliation><affiliation wicri:level="1"><nlm:aff id="af4-ijms-20-04366">Hypoxia-related Disease Research Center, College of Medicine, Inha University, Incheon 22212, Korea</nlm:aff><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Hypoxia-related Disease Research Center, College of Medicine, Inha University, Incheon 22212</wicri:regionArea><wicri:noRegion>Incheon 22212</wicri:noRegion></affiliation></author></analytic><series><title level="j">International Journal of Molecular Sciences</title><idno type="eISSN">1422-0067</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>5-Fluorouracil (5-FU) is an important chemotherapeutic agent for the systemic treatment of colorectal cancer (CRC), but its effectiveness against CRC is limited by increased 5-FU resistance caused by the hypoxic tumor microenvironment. The purpose of our study was to assess the feasibility of using quinacrine (QC) to increase the efficacy of 5-FU against CRC cells under hypoxic conditions. QC reversed the resistance to 5-FU induced by hypoxia in CRC cell lines, as determined using ATP-Glo cell viability assays and clonogenic survival assays. Treatment of cells with 5-FU under hypoxic conditions had no effect on the expression of nuclear factor (erythroid-derived 2)-like 2 (Nrf2), a regulator of cellular resistance to oxidative stress, whereas treatment with QC alone or in combination with 5-FU reduced Nrf2 expression in all CRC cell lines tested. Overexpression of Nrf2 effectively prevented the increase in the number of DNA double-strand breaks induced by QC alone or in combination with 5-FU. siRNA-mediated c-Jun <italic>N</italic>-terminal kinase-1 (JNK1) knockdown inhibited the QC-mediated Nrf2 degradation in CRC cells under hypoxic conditions. The treatment of CRC xenografts in mice with the combination of QC and 5-FU was more effective in suppressing tumor growth than QC or 5-FU alone. QC increases the susceptibility of CRC cells to 5-FU under hypoxic conditions by enhancing JNK1-dependent Nrf2 degradation.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Hammond, W A" uniqKey="Hammond W">W.A. Hammond</name></author><author><name sortKey="Swaika, A" uniqKey="Swaika A">A. Swaika</name></author><author><name sortKey="Mody, K" uniqKey="Mody K">K. Mody</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Siegel, R" uniqKey="Siegel R">R. Siegel</name></author><author><name sortKey="Ma, J" uniqKey="Ma J">J. Ma</name></author><author><name sortKey="Zou, Z" uniqKey="Zou Z">Z. Zou</name></author><author><name sortKey="Jemal, A" uniqKey="Jemal A">A. 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Motohashi</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>Corée du Sud</li></country></list><tree><noCountry><name sortKey="Kim, Chan Woo" sort="Kim, Chan Woo" uniqKey="Kim C" first="Chan Woo" last="Kim">Chan Woo Kim</name><name sortKey="Kim, Ha Gyeong" sort="Kim, Ha Gyeong" uniqKey="Kim H" first="Ha Gyeong" last="Kim">Ha Gyeong Kim</name></noCountry><country name="Corée du Sud"><noRegion><name sortKey="Lee, Don Haeng" sort="Lee, Don Haeng" uniqKey="Lee D" first="Don Haeng" last="Lee">Don Haeng Lee</name></noRegion><name sortKey="Lee, Jae Seon" sort="Lee, Jae Seon" uniqKey="Lee J" first="Jae-Seon" last="Lee">Jae-Seon Lee</name><name sortKey="Lee, Jae Seon" sort="Lee, Jae Seon" uniqKey="Lee J" first="Jae-Seon" last="Lee">Jae-Seon Lee</name><name sortKey="Oh, Eun Taex" sort="Oh, Eun Taex" uniqKey="Oh E" first="Eun-Taex" last="Oh">Eun-Taex Oh</name><name sortKey="Oh, Eun Taex" sort="Oh, Eun Taex" uniqKey="Oh E" first="Eun-Taex" last="Oh">Eun-Taex Oh</name><name sortKey="Park, Heon Joo" sort="Park, Heon Joo" uniqKey="Park H" first="Heon Joo" last="Park">Heon Joo Park</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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