IL-6 inhibits apoptosis and retains oxidative DNA lesions in human gastric cancer AGS cells through up-regulation of anti-apoptotic gene mcl-1

Apoptosis plays a critical role in maintaining genomic integrity by selectively removing the most heavily damaged cells from the population. Reactive oxygen species (ROS) and certain inflammatory cytokines are always elevated during the human carcinogenic process. However, the biological significanc...

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Veröffentlicht in:Carcinogenesis (New York) 2001-12, Vol.22 (12), p.1947-1953
Hauptverfasser: Lin, Ming-Tsan, Juan, Chiung-Yao, Chang, King-Jen, Chen, Wei-Jao, Kuo, Min-Liang
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container_end_page 1953
container_issue 12
container_start_page 1947
container_title Carcinogenesis (New York)
container_volume 22
creator Lin, Ming-Tsan
Juan, Chiung-Yao
Chang, King-Jen
Chen, Wei-Jao
Kuo, Min-Liang
description Apoptosis plays a critical role in maintaining genomic integrity by selectively removing the most heavily damaged cells from the population. Reactive oxygen species (ROS) and certain inflammatory cytokines are always elevated during the human carcinogenic process. However, the biological significance of the interplay between ROS and inflammatory cytokine remains elusive. This study demonstrates that interleukin-6 (IL-6) effectively protects gastric cancer cells from the apoptosis induced by hydrogen peroxide (H2O2). The cell death signaling JNK pathway elicited by H2O2 is also inhibited by IL-6. We further found that Mcl-1, but not other Bcl-2 family members, was up-regulated by IL-6, by a substantial level over 24 h. We further transfected a mcl-1 expression vector, pCMV-mcl-1, into the AGS cells, and successfully obtained several mcl-1-overexpressing clones. Flow cytometric analysis shows that these mcl-1-overexpressing AGS cells are more resistant to the apoptosis induced by H2O2 when compared with the neo control AGS cells. Consistently, the activation of the JNK pathway induced by H2O2 is also blocked in mcl-1-overexpressed cells. These results indicate that the anti-apoptotic effect of IL-6 is, at least in part, due to the up-regulation of mcl-1. To our surprise, either IL-6 exposure or mcl-1 overexpression fails to reduce the level of intracellular peroxides in the AGS cells triggered by H2O2. This study also determined the level of 8-hydroxydeoxyguanosine (8-OH-dGua), an indicator for oxidative DNA lesions in IL-6-treated or mcl-1-overexpressed AGS cells after treatment with H2O2. Notably, our results indicate that a majority of the 8-OH-dGua is efficiently removed in the AGS cells without IL-6 treatment, whereas only ~50% of the 8-OH-dGua was repaired in the IL-6-treated AGS cells after 24 h. Similarly, ~60–70% of the 8-OH-dGua also failed to repair and was retained in the genomic DNA of the mcl-1 transfectants. Results in this study provide a novel mechanism by which up-regulation of the Mcl-1 protein by IL-6 may enhance the susceptibility to H2O2-induced oxidative DNA lesions by overriding apoptosis.
doi_str_mv 10.1093/carcin/22.12.1947
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Reactive oxygen species (ROS) and certain inflammatory cytokines are always elevated during the human carcinogenic process. However, the biological significance of the interplay between ROS and inflammatory cytokine remains elusive. This study demonstrates that interleukin-6 (IL-6) effectively protects gastric cancer cells from the apoptosis induced by hydrogen peroxide (H2O2). The cell death signaling JNK pathway elicited by H2O2 is also inhibited by IL-6. We further found that Mcl-1, but not other Bcl-2 family members, was up-regulated by IL-6, by a substantial level over 24 h. We further transfected a mcl-1 expression vector, pCMV-mcl-1, into the AGS cells, and successfully obtained several mcl-1-overexpressing clones. Flow cytometric analysis shows that these mcl-1-overexpressing AGS cells are more resistant to the apoptosis induced by H2O2 when compared with the neo control AGS cells. Consistently, the activation of the JNK pathway induced by H2O2 is also blocked in mcl-1-overexpressed cells. These results indicate that the anti-apoptotic effect of IL-6 is, at least in part, due to the up-regulation of mcl-1. To our surprise, either IL-6 exposure or mcl-1 overexpression fails to reduce the level of intracellular peroxides in the AGS cells triggered by H2O2. This study also determined the level of 8-hydroxydeoxyguanosine (8-OH-dGua), an indicator for oxidative DNA lesions in IL-6-treated or mcl-1-overexpressed AGS cells after treatment with H2O2. Notably, our results indicate that a majority of the 8-OH-dGua is efficiently removed in the AGS cells without IL-6 treatment, whereas only ~50% of the 8-OH-dGua was repaired in the IL-6-treated AGS cells after 24 h. Similarly, ~60–70% of the 8-OH-dGua also failed to repair and was retained in the genomic DNA of the mcl-1 transfectants. Results in this study provide a novel mechanism by which up-regulation of the Mcl-1 protein by IL-6 may enhance the susceptibility to H2O2-induced oxidative DNA lesions by overriding apoptosis.</description><identifier>ISSN: 0143-3334</identifier><identifier>EISSN: 1460-2180</identifier><identifier>DOI: 10.1093/carcin/22.12.1947</identifier><identifier>PMID: 11751424</identifier><identifier>CODEN: CRNGDP</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>8-hydroxydeoxyguanosine ; 8-OH-dGua ; Ageing, cell death ; Apoptosis - drug effects ; Biological and medical sciences ; Cell physiology ; Deoxyguanosine - analogs &amp; derivatives ; Deoxyguanosine - metabolism ; DNA Damage - drug effects ; DNA Damage - genetics ; Flow Cytometry ; Fundamental and applied biological sciences. Psychology ; gastric carcinoma ; H2O2 ; Humans ; hydrogen peroxide ; Hydrogen Peroxide - pharmacology ; IL-6 ; Immunoblotting ; interleukin-6 ; Interleukin-6 - pharmacology ; JNK Mitogen-Activated Protein Kinases ; MAP Kinase Kinase 4 ; Mcl-1 protein ; Mitogen-Activated Protein Kinase Kinases - metabolism ; Molecular and cellular biology ; Myeloid Cell Leukemia Sequence 1 Protein ; Neoplasm Proteins - genetics ; Oxidative Stress - drug effects ; Proto-Oncogene Proteins c-bcl-2 ; reactive oxygen species ; ROS ; Signal Transduction - drug effects ; Stomach Neoplasms - genetics ; Stomach Neoplasms - pathology ; Time Factors ; Tumor Cells, Cultured ; Up-Regulation - drug effects</subject><ispartof>Carcinogenesis (New York), 2001-12, Vol.22 (12), p.1947-1953</ispartof><rights>2002 INIST-CNRS</rights><rights>Copyright Oxford University Press(England) Dec 2001</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c489t-ece4b3f520cb55d302b05743c49e0c3fccae5d489519f4a9c50b5e64740e7dca3</citedby><cites>FETCH-LOGICAL-c489t-ece4b3f520cb55d302b05743c49e0c3fccae5d489519f4a9c50b5e64740e7dca3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=13418913$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11751424$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lin, Ming-Tsan</creatorcontrib><creatorcontrib>Juan, Chiung-Yao</creatorcontrib><creatorcontrib>Chang, King-Jen</creatorcontrib><creatorcontrib>Chen, Wei-Jao</creatorcontrib><creatorcontrib>Kuo, Min-Liang</creatorcontrib><title>IL-6 inhibits apoptosis and retains oxidative DNA lesions in human gastric cancer AGS cells through up-regulation of anti-apoptotic gene mcl-1</title><title>Carcinogenesis (New York)</title><addtitle>Carcinogenesis</addtitle><description>Apoptosis plays a critical role in maintaining genomic integrity by selectively removing the most heavily damaged cells from the population. Reactive oxygen species (ROS) and certain inflammatory cytokines are always elevated during the human carcinogenic process. However, the biological significance of the interplay between ROS and inflammatory cytokine remains elusive. This study demonstrates that interleukin-6 (IL-6) effectively protects gastric cancer cells from the apoptosis induced by hydrogen peroxide (H2O2). The cell death signaling JNK pathway elicited by H2O2 is also inhibited by IL-6. We further found that Mcl-1, but not other Bcl-2 family members, was up-regulated by IL-6, by a substantial level over 24 h. We further transfected a mcl-1 expression vector, pCMV-mcl-1, into the AGS cells, and successfully obtained several mcl-1-overexpressing clones. Flow cytometric analysis shows that these mcl-1-overexpressing AGS cells are more resistant to the apoptosis induced by H2O2 when compared with the neo control AGS cells. Consistently, the activation of the JNK pathway induced by H2O2 is also blocked in mcl-1-overexpressed cells. These results indicate that the anti-apoptotic effect of IL-6 is, at least in part, due to the up-regulation of mcl-1. To our surprise, either IL-6 exposure or mcl-1 overexpression fails to reduce the level of intracellular peroxides in the AGS cells triggered by H2O2. This study also determined the level of 8-hydroxydeoxyguanosine (8-OH-dGua), an indicator for oxidative DNA lesions in IL-6-treated or mcl-1-overexpressed AGS cells after treatment with H2O2. Notably, our results indicate that a majority of the 8-OH-dGua is efficiently removed in the AGS cells without IL-6 treatment, whereas only ~50% of the 8-OH-dGua was repaired in the IL-6-treated AGS cells after 24 h. Similarly, ~60–70% of the 8-OH-dGua also failed to repair and was retained in the genomic DNA of the mcl-1 transfectants. Results in this study provide a novel mechanism by which up-regulation of the Mcl-1 protein by IL-6 may enhance the susceptibility to H2O2-induced oxidative DNA lesions by overriding apoptosis.</description><subject>8-hydroxydeoxyguanosine</subject><subject>8-OH-dGua</subject><subject>Ageing, cell death</subject><subject>Apoptosis - drug effects</subject><subject>Biological and medical sciences</subject><subject>Cell physiology</subject><subject>Deoxyguanosine - analogs &amp; derivatives</subject><subject>Deoxyguanosine - metabolism</subject><subject>DNA Damage - drug effects</subject><subject>DNA Damage - genetics</subject><subject>Flow Cytometry</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>gastric carcinoma</subject><subject>H2O2</subject><subject>Humans</subject><subject>hydrogen peroxide</subject><subject>Hydrogen Peroxide - pharmacology</subject><subject>IL-6</subject><subject>Immunoblotting</subject><subject>interleukin-6</subject><subject>Interleukin-6 - pharmacology</subject><subject>JNK Mitogen-Activated Protein Kinases</subject><subject>MAP Kinase Kinase 4</subject><subject>Mcl-1 protein</subject><subject>Mitogen-Activated Protein Kinase Kinases - metabolism</subject><subject>Molecular and cellular biology</subject><subject>Myeloid Cell Leukemia Sequence 1 Protein</subject><subject>Neoplasm Proteins - genetics</subject><subject>Oxidative Stress - drug effects</subject><subject>Proto-Oncogene Proteins c-bcl-2</subject><subject>reactive oxygen species</subject><subject>ROS</subject><subject>Signal Transduction - drug effects</subject><subject>Stomach Neoplasms - genetics</subject><subject>Stomach Neoplasms - pathology</subject><subject>Time Factors</subject><subject>Tumor Cells, Cultured</subject><subject>Up-Regulation - drug effects</subject><issn>0143-3334</issn><issn>1460-2180</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkV1rFDEUhoNY7Fr9Ad5IEPRu2nzObC6Xaj9gVbAVSm9CJnNmN3U2mSYZqX_C39yUWSwIBxJOnvc9h7wIvaPkmBLFT6yJ1vkTxo5pKSWaF2hBRU0qRpfkJVoQKnjFOReH6HVKd4TQmkv1Ch1S2kgqmFigv5frqsbOb13rcsJmDGMOyZWb73CEbJxPODy4zmT3G_Dnbys8QHKhdJ3H22lnPN6YlKOz2BpvIeLV-RW2MAwJ520M02aLp7GKsJmG4hE8Dn0xz66aZ-Ui3IAHvLNDRd-gg94MCd7uzyP08-zL9elFtf5-fnm6WldWLFWuwIJoeS8Zsa2UHSesJbIR3AoFxPLeWgOyK6ikqhdGWUlaCbVoBIGms4YfoU-z7xjD_QQp651LT0sbD2FKmi5ZU0tOCvjhP_AuTNGX3TSjinOlKC8QnSEbQ0oRej1GtzPxj6ZEPyWl56Q0Y5qWKkkVzfu98dTuoHtW7KMpwMc9YJI1Qx_L77r0zHFBl_PwauZcyvDw793EX7pueCP1xc2tvrq-oezH7Vd9xh8BehetnA</recordid><startdate>20011201</startdate><enddate>20011201</enddate><creator>Lin, Ming-Tsan</creator><creator>Juan, Chiung-Yao</creator><creator>Chang, King-Jen</creator><creator>Chen, Wei-Jao</creator><creator>Kuo, Min-Liang</creator><general>Oxford University Press</general><general>Oxford Publishing Limited (England)</general><scope>BSCLL</scope><scope>IQODW</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>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20011201</creationdate><title>IL-6 inhibits apoptosis and retains oxidative DNA lesions in human gastric cancer AGS cells through up-regulation of anti-apoptotic gene mcl-1</title><author>Lin, Ming-Tsan ; Juan, Chiung-Yao ; Chang, King-Jen ; Chen, Wei-Jao ; Kuo, Min-Liang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c489t-ece4b3f520cb55d302b05743c49e0c3fccae5d489519f4a9c50b5e64740e7dca3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>8-hydroxydeoxyguanosine</topic><topic>8-OH-dGua</topic><topic>Ageing, cell death</topic><topic>Apoptosis - drug effects</topic><topic>Biological and medical sciences</topic><topic>Cell physiology</topic><topic>Deoxyguanosine - analogs &amp; derivatives</topic><topic>Deoxyguanosine - metabolism</topic><topic>DNA Damage - drug effects</topic><topic>DNA Damage - genetics</topic><topic>Flow Cytometry</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>gastric carcinoma</topic><topic>H2O2</topic><topic>Humans</topic><topic>hydrogen peroxide</topic><topic>Hydrogen Peroxide - pharmacology</topic><topic>IL-6</topic><topic>Immunoblotting</topic><topic>interleukin-6</topic><topic>Interleukin-6 - pharmacology</topic><topic>JNK Mitogen-Activated Protein Kinases</topic><topic>MAP Kinase Kinase 4</topic><topic>Mcl-1 protein</topic><topic>Mitogen-Activated Protein Kinase Kinases - metabolism</topic><topic>Molecular and cellular biology</topic><topic>Myeloid Cell Leukemia Sequence 1 Protein</topic><topic>Neoplasm Proteins - genetics</topic><topic>Oxidative Stress - drug effects</topic><topic>Proto-Oncogene Proteins c-bcl-2</topic><topic>reactive oxygen species</topic><topic>ROS</topic><topic>Signal Transduction - drug effects</topic><topic>Stomach Neoplasms - genetics</topic><topic>Stomach Neoplasms - pathology</topic><topic>Time Factors</topic><topic>Tumor Cells, Cultured</topic><topic>Up-Regulation - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lin, Ming-Tsan</creatorcontrib><creatorcontrib>Juan, Chiung-Yao</creatorcontrib><creatorcontrib>Chang, King-Jen</creatorcontrib><creatorcontrib>Chen, Wei-Jao</creatorcontrib><creatorcontrib>Kuo, Min-Liang</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology 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>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Carcinogenesis (New York)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lin, Ming-Tsan</au><au>Juan, Chiung-Yao</au><au>Chang, King-Jen</au><au>Chen, Wei-Jao</au><au>Kuo, Min-Liang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>IL-6 inhibits apoptosis and retains oxidative DNA lesions in human gastric cancer AGS cells through up-regulation of anti-apoptotic gene mcl-1</atitle><jtitle>Carcinogenesis (New York)</jtitle><addtitle>Carcinogenesis</addtitle><date>2001-12-01</date><risdate>2001</risdate><volume>22</volume><issue>12</issue><spage>1947</spage><epage>1953</epage><pages>1947-1953</pages><issn>0143-3334</issn><eissn>1460-2180</eissn><coden>CRNGDP</coden><abstract>Apoptosis plays a critical role in maintaining genomic integrity by selectively removing the most heavily damaged cells from the population. Reactive oxygen species (ROS) and certain inflammatory cytokines are always elevated during the human carcinogenic process. However, the biological significance of the interplay between ROS and inflammatory cytokine remains elusive. This study demonstrates that interleukin-6 (IL-6) effectively protects gastric cancer cells from the apoptosis induced by hydrogen peroxide (H2O2). The cell death signaling JNK pathway elicited by H2O2 is also inhibited by IL-6. We further found that Mcl-1, but not other Bcl-2 family members, was up-regulated by IL-6, by a substantial level over 24 h. We further transfected a mcl-1 expression vector, pCMV-mcl-1, into the AGS cells, and successfully obtained several mcl-1-overexpressing clones. Flow cytometric analysis shows that these mcl-1-overexpressing AGS cells are more resistant to the apoptosis induced by H2O2 when compared with the neo control AGS cells. Consistently, the activation of the JNK pathway induced by H2O2 is also blocked in mcl-1-overexpressed cells. These results indicate that the anti-apoptotic effect of IL-6 is, at least in part, due to the up-regulation of mcl-1. To our surprise, either IL-6 exposure or mcl-1 overexpression fails to reduce the level of intracellular peroxides in the AGS cells triggered by H2O2. This study also determined the level of 8-hydroxydeoxyguanosine (8-OH-dGua), an indicator for oxidative DNA lesions in IL-6-treated or mcl-1-overexpressed AGS cells after treatment with H2O2. Notably, our results indicate that a majority of the 8-OH-dGua is efficiently removed in the AGS cells without IL-6 treatment, whereas only ~50% of the 8-OH-dGua was repaired in the IL-6-treated AGS cells after 24 h. Similarly, ~60–70% of the 8-OH-dGua also failed to repair and was retained in the genomic DNA of the mcl-1 transfectants. Results in this study provide a novel mechanism by which up-regulation of the Mcl-1 protein by IL-6 may enhance the susceptibility to H2O2-induced oxidative DNA lesions by overriding apoptosis.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>11751424</pmid><doi>10.1093/carcin/22.12.1947</doi><tpages>7</tpages></addata></record>
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subjects 8-hydroxydeoxyguanosine
8-OH-dGua
Ageing, cell death
Apoptosis - drug effects
Biological and medical sciences
Cell physiology
Deoxyguanosine - analogs & derivatives
Deoxyguanosine - metabolism
DNA Damage - drug effects
DNA Damage - genetics
Flow Cytometry
Fundamental and applied biological sciences. Psychology
gastric carcinoma
H2O2
Humans
hydrogen peroxide
Hydrogen Peroxide - pharmacology
IL-6
Immunoblotting
interleukin-6
Interleukin-6 - pharmacology
JNK Mitogen-Activated Protein Kinases
MAP Kinase Kinase 4
Mcl-1 protein
Mitogen-Activated Protein Kinase Kinases - metabolism
Molecular and cellular biology
Myeloid Cell Leukemia Sequence 1 Protein
Neoplasm Proteins - genetics
Oxidative Stress - drug effects
Proto-Oncogene Proteins c-bcl-2
reactive oxygen species
ROS
Signal Transduction - drug effects
Stomach Neoplasms - genetics
Stomach Neoplasms - pathology
Time Factors
Tumor Cells, Cultured
Up-Regulation - drug effects
title IL-6 inhibits apoptosis and retains oxidative DNA lesions in human gastric cancer AGS cells through up-regulation of anti-apoptotic gene mcl-1
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