Nrf2 overexpression increases the resistance of acute myeloid leukemia to cytarabine by inhibiting replication factor C4
Drug resistance is a key factor in the treatment failure of acute myeloid leukemia (AML). Nuclear factor E2-related factor 2 (Nrf2) plays a crucial role in tumor chemotherapy resistance. However, the potential mechanism of Nrf2 regulating DNA mismatch repair (MMR) pathway to mediate gene-instability...
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| Veröffentlicht in: | Cancer gene therapy 2022-11, Vol.29 (11), p.1773-1790 |
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| creator | Hu, Tianzhen Pan, Chengyun Zhang, Tianzhuo Ni, Ming Wang, Weili Zhang, Siyu Chen, Ying Wang, Jishi Fang, Qin |
| description | Drug resistance is a key factor in the treatment failure of acute myeloid leukemia (AML). Nuclear factor E2-related factor 2 (Nrf2) plays a crucial role in tumor chemotherapy resistance. However, the potential mechanism of Nrf2 regulating DNA mismatch repair (MMR) pathway to mediate gene-instability drug resistance in AML is still unclear. Here, it was found that Nrf2 expression was closely related to the disease progression of AML as well as highly expressed in AML patients with poor prognostic gene mutations. Meanwhile, it was also found that the expression of Nrf2 was significantly negatively correlated with DNA MMR gene replication factor C4 (RFC4) in AML. CHIP analysis combined with luciferase reporter gene results further showed that Nrf2 may inhibit the expression of RFC4 by its interaction with the RFC4 promoter. In vitro and vivo experiments showed that the overexpression of Nrf2 decreased the killing effect of chemotherapy drug cytarabine (Ara-C) on leukemia cells and inhibited the expression of RFC4. Mechanistically, The result that Nrf2-RFC4 axis mediated AML genetic instability drug resistance might be received by activating the JNK/NF-κB signaling pathway. Taken together, these findings may provide a new idea for improving AML drug resistance. |
| doi_str_mv | 10.1038/s41417-022-00501-1 |
| format | Article |
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Nuclear factor E2-related factor 2 (Nrf2) plays a crucial role in tumor chemotherapy resistance. However, the potential mechanism of Nrf2 regulating DNA mismatch repair (MMR) pathway to mediate gene-instability drug resistance in AML is still unclear. Here, it was found that Nrf2 expression was closely related to the disease progression of AML as well as highly expressed in AML patients with poor prognostic gene mutations. Meanwhile, it was also found that the expression of Nrf2 was significantly negatively correlated with DNA MMR gene replication factor C4 (RFC4) in AML. CHIP analysis combined with luciferase reporter gene results further showed that Nrf2 may inhibit the expression of RFC4 by its interaction with the RFC4 promoter. In vitro and vivo experiments showed that the overexpression of Nrf2 decreased the killing effect of chemotherapy drug cytarabine (Ara-C) on leukemia cells and inhibited the expression of RFC4. Mechanistically, The result that Nrf2-RFC4 axis mediated AML genetic instability drug resistance might be received by activating the JNK/NF-κB signaling pathway. Taken together, these findings may provide a new idea for improving AML drug resistance.</description><identifier>ISSN: 0929-1903</identifier><identifier>EISSN: 1476-5500</identifier><identifier>DOI: 10.1038/s41417-022-00501-1</identifier><identifier>PMID: 35840666</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>13/1 ; 13/2 ; 13/31 ; 13/51 ; 14/1 ; 14/35 ; 14/63 ; 38/1 ; 38/35 ; 631/208/199 ; 631/67/1990/283 ; Acute myeloid leukemia ; Biomedical and Life Sciences ; Biomedicine ; Cell Line, Tumor ; Chemoresistance ; Chemotherapy ; Cytarabine ; Cytarabine - pharmacology ; Cytarabine - therapeutic use ; DNA biosynthesis ; DNA repair ; Drug resistance ; Drug Resistance, Neoplasm - genetics ; Gene Expression ; Gene Therapy ; Genomic instability ; Humans ; Leukemia ; Leukemia, Myeloid, Acute - drug therapy ; Leukemia, Myeloid, Acute - genetics ; Leukemia, Myeloid, Acute - pathology ; Mismatch repair ; NF-E2-Related Factor 2 - genetics ; NF-E2-Related Factor 2 - metabolism ; NF-kappa B - metabolism ; NF-κB protein ; Replication ; Reporter gene ; Signal transduction ; Tumors</subject><ispartof>Cancer gene therapy, 2022-11, Vol.29 (11), p.1773-1790</ispartof><rights>The Author(s) 2022. corrected publication 2022</rights><rights>2022. The Author(s).</rights><rights>The Author(s) 2022. corrected publication 2022. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The Author(s) 2022, corrected publication 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-a6b933aa8831d9b71dd64b7eca455eaff0b014f2443af1bb6d40fef053e242693</citedby><cites>FETCH-LOGICAL-c474t-a6b933aa8831d9b71dd64b7eca455eaff0b014f2443af1bb6d40fef053e242693</cites><orcidid>0000-0001-5118-6990 ; 0000-0002-8642-3447 ; 0000-0001-9492-5204</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/s41417-022-00501-1$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/s41417-022-00501-1$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,780,784,885,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35840666$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hu, Tianzhen</creatorcontrib><creatorcontrib>Pan, Chengyun</creatorcontrib><creatorcontrib>Zhang, Tianzhuo</creatorcontrib><creatorcontrib>Ni, Ming</creatorcontrib><creatorcontrib>Wang, Weili</creatorcontrib><creatorcontrib>Zhang, Siyu</creatorcontrib><creatorcontrib>Chen, Ying</creatorcontrib><creatorcontrib>Wang, Jishi</creatorcontrib><creatorcontrib>Fang, Qin</creatorcontrib><title>Nrf2 overexpression increases the resistance of acute myeloid leukemia to cytarabine by inhibiting replication factor C4</title><title>Cancer gene therapy</title><addtitle>Cancer Gene Ther</addtitle><addtitle>Cancer Gene Ther</addtitle><description>Drug resistance is a key factor in the treatment failure of acute myeloid leukemia (AML). Nuclear factor E2-related factor 2 (Nrf2) plays a crucial role in tumor chemotherapy resistance. However, the potential mechanism of Nrf2 regulating DNA mismatch repair (MMR) pathway to mediate gene-instability drug resistance in AML is still unclear. Here, it was found that Nrf2 expression was closely related to the disease progression of AML as well as highly expressed in AML patients with poor prognostic gene mutations. Meanwhile, it was also found that the expression of Nrf2 was significantly negatively correlated with DNA MMR gene replication factor C4 (RFC4) in AML. CHIP analysis combined with luciferase reporter gene results further showed that Nrf2 may inhibit the expression of RFC4 by its interaction with the RFC4 promoter. In vitro and vivo experiments showed that the overexpression of Nrf2 decreased the killing effect of chemotherapy drug cytarabine (Ara-C) on leukemia cells and inhibited the expression of RFC4. Mechanistically, The result that Nrf2-RFC4 axis mediated AML genetic instability drug resistance might be received by activating the JNK/NF-κB signaling pathway. Taken together, these findings may provide a new idea for improving AML drug resistance.</description><subject>13/1</subject><subject>13/2</subject><subject>13/31</subject><subject>13/51</subject><subject>14/1</subject><subject>14/35</subject><subject>14/63</subject><subject>38/1</subject><subject>38/35</subject><subject>631/208/199</subject><subject>631/67/1990/283</subject><subject>Acute myeloid leukemia</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Line, Tumor</subject><subject>Chemoresistance</subject><subject>Chemotherapy</subject><subject>Cytarabine</subject><subject>Cytarabine - pharmacology</subject><subject>Cytarabine - therapeutic use</subject><subject>DNA biosynthesis</subject><subject>DNA repair</subject><subject>Drug resistance</subject><subject>Drug Resistance, Neoplasm - genetics</subject><subject>Gene Expression</subject><subject>Gene Therapy</subject><subject>Genomic instability</subject><subject>Humans</subject><subject>Leukemia</subject><subject>Leukemia, Myeloid, Acute - drug therapy</subject><subject>Leukemia, Myeloid, Acute - genetics</subject><subject>Leukemia, Myeloid, Acute - pathology</subject><subject>Mismatch repair</subject><subject>NF-E2-Related Factor 2 - genetics</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB protein</subject><subject>Replication</subject><subject>Reporter gene</subject><subject>Signal transduction</subject><subject>Tumors</subject><issn>0929-1903</issn><issn>1476-5500</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kU9vEzEQxS0EoqHwBTggS5y3-N96sxckFAFFquACZ2vsHScuGzvY3qr59rikFLhwGmnem9_M6BHykrMLzuT6TVFc8aFjQnSM9Yx3_BFZcTXoru8Ze0xWbBRjx0cmz8izUq4Za-Ign5Iz2a8V01qvyO3n7AVNN5jx9pCxlJAiDdFlhIKF1h3S1g2lQnRIk6fglop0f8Q5hYnOuHzHfQBaE3XHChlsiEjtsTF2wYYa4rYBDnNwUO_QHlxNmW7Uc_LEw1zwxX09J98-vP-6ueyuvnz8tHl31Tk1qNqBtqOUAOu15NNoBz5NWtkBHai-R_Ce2faVF0pJ8NxaPSnm0bNeolBCj_KcvD1xD4vd4-Qw1gyzOeSwh3w0CYL5V4lhZ7bpxoxaSzHqBnh9D8jpx4Klmuu05NhuNmKQmg2Sa9Fc4uRyOZWS0T9s4MzcpWVOaZmWlvmVluFt6NXftz2M_I6nGeTJUJoUt5j_7P4P9ic7yqOB</recordid><startdate>20221101</startdate><enddate>20221101</enddate><creator>Hu, Tianzhen</creator><creator>Pan, Chengyun</creator><creator>Zhang, Tianzhuo</creator><creator>Ni, Ming</creator><creator>Wang, Weili</creator><creator>Zhang, Siyu</creator><creator>Chen, Ying</creator><creator>Wang, Jishi</creator><creator>Fang, Qin</creator><general>Nature Publishing Group US</general><general>Nature Publishing Group</general><scope>C6C</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-5118-6990</orcidid><orcidid>https://orcid.org/0000-0002-8642-3447</orcidid><orcidid>https://orcid.org/0000-0001-9492-5204</orcidid></search><sort><creationdate>20221101</creationdate><title>Nrf2 overexpression increases the resistance of acute myeloid leukemia to cytarabine by inhibiting replication factor C4</title><author>Hu, Tianzhen ; Pan, Chengyun ; Zhang, Tianzhuo ; Ni, Ming ; Wang, Weili ; Zhang, Siyu ; Chen, Ying ; Wang, Jishi ; Fang, Qin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-a6b933aa8831d9b71dd64b7eca455eaff0b014f2443af1bb6d40fef053e242693</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>13/1</topic><topic>13/2</topic><topic>13/31</topic><topic>13/51</topic><topic>14/1</topic><topic>14/35</topic><topic>14/63</topic><topic>38/1</topic><topic>38/35</topic><topic>631/208/199</topic><topic>631/67/1990/283</topic><topic>Acute myeloid leukemia</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell Line, Tumor</topic><topic>Chemoresistance</topic><topic>Chemotherapy</topic><topic>Cytarabine</topic><topic>Cytarabine - pharmacology</topic><topic>Cytarabine - therapeutic use</topic><topic>DNA biosynthesis</topic><topic>DNA repair</topic><topic>Drug resistance</topic><topic>Drug Resistance, Neoplasm - genetics</topic><topic>Gene Expression</topic><topic>Gene Therapy</topic><topic>Genomic instability</topic><topic>Humans</topic><topic>Leukemia</topic><topic>Leukemia, Myeloid, Acute - drug therapy</topic><topic>Leukemia, Myeloid, Acute - genetics</topic><topic>Leukemia, Myeloid, Acute - pathology</topic><topic>Mismatch repair</topic><topic>NF-E2-Related Factor 2 - genetics</topic><topic>NF-E2-Related Factor 2 - metabolism</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB protein</topic><topic>Replication</topic><topic>Reporter gene</topic><topic>Signal transduction</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hu, Tianzhen</creatorcontrib><creatorcontrib>Pan, Chengyun</creatorcontrib><creatorcontrib>Zhang, Tianzhuo</creatorcontrib><creatorcontrib>Ni, Ming</creatorcontrib><creatorcontrib>Wang, Weili</creatorcontrib><creatorcontrib>Zhang, Siyu</creatorcontrib><creatorcontrib>Chen, Ying</creatorcontrib><creatorcontrib>Wang, Jishi</creatorcontrib><creatorcontrib>Fang, Qin</creatorcontrib><collection>Springer Nature OA/Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancer gene therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hu, Tianzhen</au><au>Pan, Chengyun</au><au>Zhang, Tianzhuo</au><au>Ni, Ming</au><au>Wang, Weili</au><au>Zhang, Siyu</au><au>Chen, Ying</au><au>Wang, Jishi</au><au>Fang, Qin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Nrf2 overexpression increases the resistance of acute myeloid leukemia to cytarabine by inhibiting replication factor C4</atitle><jtitle>Cancer gene therapy</jtitle><stitle>Cancer Gene Ther</stitle><addtitle>Cancer Gene Ther</addtitle><date>2022-11-01</date><risdate>2022</risdate><volume>29</volume><issue>11</issue><spage>1773</spage><epage>1790</epage><pages>1773-1790</pages><issn>0929-1903</issn><eissn>1476-5500</eissn><abstract>Drug resistance is a key factor in the treatment failure of acute myeloid leukemia (AML). Nuclear factor E2-related factor 2 (Nrf2) plays a crucial role in tumor chemotherapy resistance. However, the potential mechanism of Nrf2 regulating DNA mismatch repair (MMR) pathway to mediate gene-instability drug resistance in AML is still unclear. Here, it was found that Nrf2 expression was closely related to the disease progression of AML as well as highly expressed in AML patients with poor prognostic gene mutations. Meanwhile, it was also found that the expression of Nrf2 was significantly negatively correlated with DNA MMR gene replication factor C4 (RFC4) in AML. CHIP analysis combined with luciferase reporter gene results further showed that Nrf2 may inhibit the expression of RFC4 by its interaction with the RFC4 promoter. In vitro and vivo experiments showed that the overexpression of Nrf2 decreased the killing effect of chemotherapy drug cytarabine (Ara-C) on leukemia cells and inhibited the expression of RFC4. Mechanistically, The result that Nrf2-RFC4 axis mediated AML genetic instability drug resistance might be received by activating the JNK/NF-κB signaling pathway. Taken together, these findings may provide a new idea for improving AML drug resistance.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>35840666</pmid><doi>10.1038/s41417-022-00501-1</doi><tpages>18</tpages><orcidid>https://orcid.org/0000-0001-5118-6990</orcidid><orcidid>https://orcid.org/0000-0002-8642-3447</orcidid><orcidid>https://orcid.org/0000-0001-9492-5204</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | 13/1 13/2 13/31 13/51 14/1 14/35 14/63 38/1 38/35 631/208/199 631/67/1990/283 Acute myeloid leukemia Biomedical and Life Sciences Biomedicine Cell Line, Tumor Chemoresistance Chemotherapy Cytarabine Cytarabine - pharmacology Cytarabine - therapeutic use DNA biosynthesis DNA repair Drug resistance Drug Resistance, Neoplasm - genetics Gene Expression Gene Therapy Genomic instability Humans Leukemia Leukemia, Myeloid, Acute - drug therapy Leukemia, Myeloid, Acute - genetics Leukemia, Myeloid, Acute - pathology Mismatch repair NF-E2-Related Factor 2 - genetics NF-E2-Related Factor 2 - metabolism NF-kappa B - metabolism NF-κB protein Replication Reporter gene Signal transduction Tumors |
| title | Nrf2 overexpression increases the resistance of acute myeloid leukemia to cytarabine by inhibiting replication factor C4 |
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