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Glutathione reductase mediates drug resistance in glioblastoma cells by regulating redox homeostasis
Glutathione (GSH) and GSH‐related enzymes constitute the most important defense system that protects cells from free radical, radiotherapy, and chemotherapy attacks. In this study, we aim to explore the potential role and regulatory mechanism of the GSH redox cycle in drug resistance in glioblastoma...
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Published in: | Journal of neurochemistry 2018-01, Vol.144 (1), p.93-104 |
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description | Glutathione (GSH) and GSH‐related enzymes constitute the most important defense system that protects cells from free radical, radiotherapy, and chemotherapy attacks. In this study, we aim to explore the potential role and regulatory mechanism of the GSH redox cycle in drug resistance in glioblastoma multiforme (GBM) cells. We found that temozolomide (TMZ)‐resistant glioma cells displayed lower levels of endogenous reactive oxygen species and higher levels of total antioxidant capacity and GSH than sensitive cells. Moreover, the expression of glutathione reductase (GSR), the key enzyme of the GSH redox cycle, was higher in TMZ‐resistant cells than in sensitive cells. Furthermore, silencing GSR in drug‐resistant cells improved the sensitivity of cells to TMZ or cisplatin. Conversely, the over‐expression of GSR in sensitive cells resulted in resistance to chemotherapy. In addition, the GSR enzyme partially prevented the oxidative stress caused by pro‐oxidant L‐buthionine ‐sulfoximine. The modulation of redox state by GSH or L‐buthionine –sulfoximine regulated GSR‐mediated drug resistance, suggesting that the action of GSR in drug resistance is associated with the modulation of redox homeostasis. Intriguingly, a trend toward shorter progress‐free survival was observed among GBM patients with high GSR expression. These results indicated that GSR is involved in mediating drug resistance and is a potential target for improving GBM treatment.
Glioblastoma multiforme is the most aggressive type of brain tumor. We show that glutathione reductase (GSR), the key enzyme of the glutathione (GSH) redox cycle, mediates drug resistance by regulating redox homeostasis and is a potential target for improving GBM treatment. These findings provide new ideas and strategies for reversing drug resistance. |
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Glioblastoma multiforme is the most aggressive type of brain tumor. We show that glutathione reductase (GSR), the key enzyme of the glutathione (GSH) redox cycle, mediates drug resistance by regulating redox homeostasis and is a potential target for improving GBM treatment. These findings provide new ideas and strategies for reversing drug resistance.</description><identifier>ISSN: 0022-3042</identifier><identifier>EISSN: 1471-4159</identifier><identifier>DOI: 10.1111/jnc.14250</identifier><identifier>PMID: 29105080</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>Animals ; Antineoplastic Agents - pharmacology ; Antineoplastic Agents - therapeutic use ; Antioxidants ; Brain cancer ; Brain Neoplasms - drug therapy ; Brain Neoplasms - enzymology ; Brain Neoplasms - mortality ; Brain Neoplasms - pathology ; Brain tumors ; Buthionine Sulfoximine - pharmacology ; Cell Line, Tumor ; Chemotherapy ; Cisplatin ; Cisplatin - pharmacology ; Cisplatin - therapeutic use ; Dacarbazine - analogs & derivatives ; Dacarbazine - pharmacology ; Dacarbazine - therapeutic use ; Disease-Free Survival ; Drug resistance ; Drug Resistance, Neoplasm ; Enzymes ; Female ; Gene Knockdown Techniques ; Glioblastoma ; Glioblastoma - drug therapy ; Glioblastoma - enzymology ; Glioblastoma - mortality ; Glioblastoma - pathology ; Glioblastoma cells ; Glioma cells ; Glutathione ; Glutathione - metabolism ; Glutathione reductase ; Glutathione Reductase - antagonists & inhibitors ; Glutathione Reductase - biosynthesis ; Glutathione Reductase - genetics ; Glutathione Reductase - physiology ; Homeostasis ; Humans ; Mice ; Mice, Inbred BALB C ; Modulation ; Neoplasm Proteins - antagonists & inhibitors ; Neoplasm Proteins - biosynthesis ; Neoplasm Proteins - genetics ; Neoplasm Proteins - physiology ; Overexpression ; Oxidants - pharmacology ; Oxidation resistance ; Oxidation-Reduction ; Oxidative Stress ; Radiation therapy ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; redox homeostasis ; Redox properties ; Regulatory mechanisms (biology) ; resistance ; RNA, Small Interfering - pharmacology ; Temozolomide ; Tumor Stem Cell Assay ; Xenograft Model Antitumor Assays</subject><ispartof>Journal of neurochemistry, 2018-01, Vol.144 (1), p.93-104</ispartof><rights>2017 International Society for Neurochemistry</rights><rights>2017 International Society for Neurochemistry.</rights><rights>Copyright © 2018 International Society for Neurochemistry</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4540-17b1be0c2546811ba14703f1185c03c85949cb5852c7e0bc38c29959759e8b1b3</citedby><cites>FETCH-LOGICAL-c4540-17b1be0c2546811ba14703f1185c03c85949cb5852c7e0bc38c29959759e8b1b3</cites><orcidid>0000-0001-8465-1414 ; 0000-0002-3691-9823</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29105080$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhu, Zhongling</creatorcontrib><creatorcontrib>Du, Shuangshuang</creatorcontrib><creatorcontrib>Du, Yibo</creatorcontrib><creatorcontrib>Ren, Jing</creatorcontrib><creatorcontrib>Ying, Guoguang</creatorcontrib><creatorcontrib>Yan, Zhao</creatorcontrib><title>Glutathione reductase mediates drug resistance in glioblastoma cells by regulating redox homeostasis</title><title>Journal of neurochemistry</title><addtitle>J Neurochem</addtitle><description>Glutathione (GSH) and GSH‐related enzymes constitute the most important defense system that protects cells from free radical, radiotherapy, and chemotherapy attacks. In this study, we aim to explore the potential role and regulatory mechanism of the GSH redox cycle in drug resistance in glioblastoma multiforme (GBM) cells. We found that temozolomide (TMZ)‐resistant glioma cells displayed lower levels of endogenous reactive oxygen species and higher levels of total antioxidant capacity and GSH than sensitive cells. Moreover, the expression of glutathione reductase (GSR), the key enzyme of the GSH redox cycle, was higher in TMZ‐resistant cells than in sensitive cells. Furthermore, silencing GSR in drug‐resistant cells improved the sensitivity of cells to TMZ or cisplatin. Conversely, the over‐expression of GSR in sensitive cells resulted in resistance to chemotherapy. In addition, the GSR enzyme partially prevented the oxidative stress caused by pro‐oxidant L‐buthionine ‐sulfoximine. The modulation of redox state by GSH or L‐buthionine –sulfoximine regulated GSR‐mediated drug resistance, suggesting that the action of GSR in drug resistance is associated with the modulation of redox homeostasis. Intriguingly, a trend toward shorter progress‐free survival was observed among GBM patients with high GSR expression. These results indicated that GSR is involved in mediating drug resistance and is a potential target for improving GBM treatment.
Glioblastoma multiforme is the most aggressive type of brain tumor. We show that glutathione reductase (GSR), the key enzyme of the glutathione (GSH) redox cycle, mediates drug resistance by regulating redox homeostasis and is a potential target for improving GBM treatment. These findings provide new ideas and strategies for reversing drug resistance.</description><subject>Animals</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>Antioxidants</subject><subject>Brain cancer</subject><subject>Brain Neoplasms - drug therapy</subject><subject>Brain Neoplasms - enzymology</subject><subject>Brain Neoplasms - mortality</subject><subject>Brain Neoplasms - pathology</subject><subject>Brain tumors</subject><subject>Buthionine Sulfoximine - pharmacology</subject><subject>Cell Line, Tumor</subject><subject>Chemotherapy</subject><subject>Cisplatin</subject><subject>Cisplatin - pharmacology</subject><subject>Cisplatin - therapeutic use</subject><subject>Dacarbazine - analogs & derivatives</subject><subject>Dacarbazine - pharmacology</subject><subject>Dacarbazine - therapeutic use</subject><subject>Disease-Free Survival</subject><subject>Drug resistance</subject><subject>Drug Resistance, Neoplasm</subject><subject>Enzymes</subject><subject>Female</subject><subject>Gene Knockdown Techniques</subject><subject>Glioblastoma</subject><subject>Glioblastoma - drug therapy</subject><subject>Glioblastoma - enzymology</subject><subject>Glioblastoma - mortality</subject><subject>Glioblastoma - pathology</subject><subject>Glioblastoma cells</subject><subject>Glioma cells</subject><subject>Glutathione</subject><subject>Glutathione - metabolism</subject><subject>Glutathione reductase</subject><subject>Glutathione Reductase - antagonists & inhibitors</subject><subject>Glutathione Reductase - biosynthesis</subject><subject>Glutathione Reductase - genetics</subject><subject>Glutathione Reductase - physiology</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Modulation</subject><subject>Neoplasm Proteins - antagonists & inhibitors</subject><subject>Neoplasm Proteins - biosynthesis</subject><subject>Neoplasm Proteins - genetics</subject><subject>Neoplasm Proteins - physiology</subject><subject>Overexpression</subject><subject>Oxidants - pharmacology</subject><subject>Oxidation resistance</subject><subject>Oxidation-Reduction</subject><subject>Oxidative Stress</subject><subject>Radiation therapy</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>redox homeostasis</subject><subject>Redox properties</subject><subject>Regulatory mechanisms (biology)</subject><subject>resistance</subject><subject>RNA, Small Interfering - pharmacology</subject><subject>Temozolomide</subject><subject>Tumor Stem Cell Assay</subject><subject>Xenograft Model Antitumor Assays</subject><issn>0022-3042</issn><issn>1471-4159</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNp10EFLwzAUB_AgipvTg19ACl70UPdemzTNUYZOZehFzyVNsy2jbWbToPv2Zm56EMwlEH7vz8ufkHOEGwxnvGrVDdKEwQEZIuUYU2TikAwBkiROgSYDcuLcCgAzmuExGSQCgUEOQ1JNa9_Lfmlsq6NOV1710umo0ZWRvXZR1flFeHfG9bJVOjJttKiNLWvpetvISOm6dlG5CWbha9mbdssr-xktbaNtmAqjp-RoLmunz_b3iLzd371OHuLZy_RxcjuLFWUUYuQllhpUwmiWI5Yy_AXSOWLOFKQqZ4IKVbKcJYprKFWaq0QIJjgTOg-j6Yhc7XLXnX332vVFY9x2Q9lq612BIkNIWSbyQC__0JX1XRu2C4pznjFAHtT1TqnOOtfpebHuTCO7TYFQbKsvQvXFd_XBXuwTfRnq-5U_XQcw3oEPU-vN_0nF0_NkF_kFyCmNDg</recordid><startdate>201801</startdate><enddate>201801</enddate><creator>Zhu, Zhongling</creator><creator>Du, Shuangshuang</creator><creator>Du, Yibo</creator><creator>Ren, Jing</creator><creator>Ying, Guoguang</creator><creator>Yan, Zhao</creator><general>Blackwell Publishing Ltd</general><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>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-8465-1414</orcidid><orcidid>https://orcid.org/0000-0002-3691-9823</orcidid></search><sort><creationdate>201801</creationdate><title>Glutathione reductase mediates drug resistance in glioblastoma cells by regulating redox homeostasis</title><author>Zhu, Zhongling ; Du, Shuangshuang ; Du, Yibo ; Ren, Jing ; Ying, Guoguang ; Yan, Zhao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4540-17b1be0c2546811ba14703f1185c03c85949cb5852c7e0bc38c29959759e8b1b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animals</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Antineoplastic Agents - therapeutic use</topic><topic>Antioxidants</topic><topic>Brain cancer</topic><topic>Brain Neoplasms - drug therapy</topic><topic>Brain Neoplasms - enzymology</topic><topic>Brain Neoplasms - mortality</topic><topic>Brain Neoplasms - pathology</topic><topic>Brain tumors</topic><topic>Buthionine Sulfoximine - pharmacology</topic><topic>Cell Line, Tumor</topic><topic>Chemotherapy</topic><topic>Cisplatin</topic><topic>Cisplatin - pharmacology</topic><topic>Cisplatin - therapeutic use</topic><topic>Dacarbazine - analogs & derivatives</topic><topic>Dacarbazine - pharmacology</topic><topic>Dacarbazine - therapeutic use</topic><topic>Disease-Free Survival</topic><topic>Drug resistance</topic><topic>Drug Resistance, Neoplasm</topic><topic>Enzymes</topic><topic>Female</topic><topic>Gene Knockdown Techniques</topic><topic>Glioblastoma</topic><topic>Glioblastoma - drug therapy</topic><topic>Glioblastoma - enzymology</topic><topic>Glioblastoma - mortality</topic><topic>Glioblastoma - pathology</topic><topic>Glioblastoma cells</topic><topic>Glioma cells</topic><topic>Glutathione</topic><topic>Glutathione - metabolism</topic><topic>Glutathione reductase</topic><topic>Glutathione Reductase - antagonists & inhibitors</topic><topic>Glutathione Reductase - biosynthesis</topic><topic>Glutathione Reductase - genetics</topic><topic>Glutathione Reductase - physiology</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Modulation</topic><topic>Neoplasm Proteins - antagonists & inhibitors</topic><topic>Neoplasm Proteins - biosynthesis</topic><topic>Neoplasm Proteins - genetics</topic><topic>Neoplasm Proteins - physiology</topic><topic>Overexpression</topic><topic>Oxidants - pharmacology</topic><topic>Oxidation resistance</topic><topic>Oxidation-Reduction</topic><topic>Oxidative Stress</topic><topic>Radiation therapy</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>redox homeostasis</topic><topic>Redox properties</topic><topic>Regulatory mechanisms (biology)</topic><topic>resistance</topic><topic>RNA, Small Interfering - pharmacology</topic><topic>Temozolomide</topic><topic>Tumor Stem Cell Assay</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhu, Zhongling</creatorcontrib><creatorcontrib>Du, Shuangshuang</creatorcontrib><creatorcontrib>Du, Yibo</creatorcontrib><creatorcontrib>Ren, Jing</creatorcontrib><creatorcontrib>Ying, Guoguang</creatorcontrib><creatorcontrib>Yan, Zhao</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of neurochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhu, Zhongling</au><au>Du, Shuangshuang</au><au>Du, Yibo</au><au>Ren, Jing</au><au>Ying, Guoguang</au><au>Yan, Zhao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Glutathione reductase mediates drug resistance in glioblastoma cells by regulating redox homeostasis</atitle><jtitle>Journal of neurochemistry</jtitle><addtitle>J Neurochem</addtitle><date>2018-01</date><risdate>2018</risdate><volume>144</volume><issue>1</issue><spage>93</spage><epage>104</epage><pages>93-104</pages><issn>0022-3042</issn><eissn>1471-4159</eissn><abstract>Glutathione (GSH) and GSH‐related enzymes constitute the most important defense system that protects cells from free radical, radiotherapy, and chemotherapy attacks. In this study, we aim to explore the potential role and regulatory mechanism of the GSH redox cycle in drug resistance in glioblastoma multiforme (GBM) cells. We found that temozolomide (TMZ)‐resistant glioma cells displayed lower levels of endogenous reactive oxygen species and higher levels of total antioxidant capacity and GSH than sensitive cells. Moreover, the expression of glutathione reductase (GSR), the key enzyme of the GSH redox cycle, was higher in TMZ‐resistant cells than in sensitive cells. Furthermore, silencing GSR in drug‐resistant cells improved the sensitivity of cells to TMZ or cisplatin. Conversely, the over‐expression of GSR in sensitive cells resulted in resistance to chemotherapy. In addition, the GSR enzyme partially prevented the oxidative stress caused by pro‐oxidant L‐buthionine ‐sulfoximine. The modulation of redox state by GSH or L‐buthionine –sulfoximine regulated GSR‐mediated drug resistance, suggesting that the action of GSR in drug resistance is associated with the modulation of redox homeostasis. Intriguingly, a trend toward shorter progress‐free survival was observed among GBM patients with high GSR expression. These results indicated that GSR is involved in mediating drug resistance and is a potential target for improving GBM treatment.
Glioblastoma multiforme is the most aggressive type of brain tumor. We show that glutathione reductase (GSR), the key enzyme of the glutathione (GSH) redox cycle, mediates drug resistance by regulating redox homeostasis and is a potential target for improving GBM treatment. These findings provide new ideas and strategies for reversing drug resistance.</abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>29105080</pmid><doi>10.1111/jnc.14250</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0001-8465-1414</orcidid><orcidid>https://orcid.org/0000-0002-3691-9823</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Animals Antineoplastic Agents - pharmacology Antineoplastic Agents - therapeutic use Antioxidants Brain cancer Brain Neoplasms - drug therapy Brain Neoplasms - enzymology Brain Neoplasms - mortality Brain Neoplasms - pathology Brain tumors Buthionine Sulfoximine - pharmacology Cell Line, Tumor Chemotherapy Cisplatin Cisplatin - pharmacology Cisplatin - therapeutic use Dacarbazine - analogs & derivatives Dacarbazine - pharmacology Dacarbazine - therapeutic use Disease-Free Survival Drug resistance Drug Resistance, Neoplasm Enzymes Female Gene Knockdown Techniques Glioblastoma Glioblastoma - drug therapy Glioblastoma - enzymology Glioblastoma - mortality Glioblastoma - pathology Glioblastoma cells Glioma cells Glutathione Glutathione - metabolism Glutathione reductase Glutathione Reductase - antagonists & inhibitors Glutathione Reductase - biosynthesis Glutathione Reductase - genetics Glutathione Reductase - physiology Homeostasis Humans Mice Mice, Inbred BALB C Modulation Neoplasm Proteins - antagonists & inhibitors Neoplasm Proteins - biosynthesis Neoplasm Proteins - genetics Neoplasm Proteins - physiology Overexpression Oxidants - pharmacology Oxidation resistance Oxidation-Reduction Oxidative Stress Radiation therapy Reactive oxygen species Reactive Oxygen Species - metabolism redox homeostasis Redox properties Regulatory mechanisms (biology) resistance RNA, Small Interfering - pharmacology Temozolomide Tumor Stem Cell Assay Xenograft Model Antitumor Assays |
title | Glutathione reductase mediates drug resistance in glioblastoma cells by regulating redox homeostasis |
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