Correlation of Reactive Oxygen Species Levels with Resveratrol Sensitivities of Anaplastic Thyroid Cancer Cells
Anaplastic thyroid carcinoma (ATC) is the most lethal thyroid malignancy without a reliable therapeutic agent. Resveratrol possesses cancer-suppressive effects, while its effect(s) on ATC cells remains unknown. Because oxidative damage caused by increased reactive oxygen species (ROS) is one of the...
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| creator | Liu, Jia Kong, Qing-You Wu, Mo-Li Song, Xue Tian, Xiao-Ting Jia, Bin Zheng, Xu Li, Hong |
| description | Anaplastic thyroid carcinoma (ATC) is the most lethal thyroid malignancy without a reliable therapeutic agent. Resveratrol possesses cancer-suppressive effects, while its effect(s) on ATC cells remains unknown. Because oxidative damage caused by increased reactive oxygen species (ROS) is one of the therapeutic effects of anticancer drugs and oxidative stress-caused mitochondria swelling is observed in resveratrol-treated cancer cells, the oxidative statuses and their relevance with resveratrol sensitivities are elucidated using THJ-16T and THJ-11T ATC cells established from two human anaplastic thyroid carcinoma cases. The results revealed that resveratrol-treated THJ-16T rather than THJ-11T cells showed remarkable growth arrest and extensive apoptosis accompanied with the elevated ROS generation and the attenuated superoxide dismutase 2 (SOD2) and catalase (CAT) levels. Mitochondrial impairment and the enhanced caspase-9/caspase-3 activation are found only in resveratrol-sensitive THJ-16T cells. Treatment with the antioxidant N-acetylcysteine (NAC) partly attenuated resveratrol-induced ROS generation and apoptosis of THJ-16T cells. The levels of resveratrol metabolic enzymes (SULT1A1 and SULT1C2) in THJ-16T cells were lower than those in THJ-11T cells and therefore reversely related with resveratrol sensitivities of ATC cells. Our findings demonstrate the ability of resveratrol to increase ROS generation and oxidative-related cellular lesions in resveratrol-sensitive THJ-16T cells presumably through activating the ROS-mitochondrial signal pathway. The levels of SULTs and ROS may reflect the response manners of ATC cells to resveratrol. |
| doi_str_mv | 10.1155/2018/6235417 |
| format | Article |
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Resveratrol possesses cancer-suppressive effects, while its effect(s) on ATC cells remains unknown. Because oxidative damage caused by increased reactive oxygen species (ROS) is one of the therapeutic effects of anticancer drugs and oxidative stress-caused mitochondria swelling is observed in resveratrol-treated cancer cells, the oxidative statuses and their relevance with resveratrol sensitivities are elucidated using THJ-16T and THJ-11T ATC cells established from two human anaplastic thyroid carcinoma cases. The results revealed that resveratrol-treated THJ-16T rather than THJ-11T cells showed remarkable growth arrest and extensive apoptosis accompanied with the elevated ROS generation and the attenuated superoxide dismutase 2 (SOD2) and catalase (CAT) levels. Mitochondrial impairment and the enhanced caspase-9/caspase-3 activation are found only in resveratrol-sensitive THJ-16T cells. Treatment with the antioxidant N-acetylcysteine (NAC) partly attenuated resveratrol-induced ROS generation and apoptosis of THJ-16T cells. The levels of resveratrol metabolic enzymes (SULT1A1 and SULT1C2) in THJ-16T cells were lower than those in THJ-11T cells and therefore reversely related with resveratrol sensitivities of ATC cells. Our findings demonstrate the ability of resveratrol to increase ROS generation and oxidative-related cellular lesions in resveratrol-sensitive THJ-16T cells presumably through activating the ROS-mitochondrial signal pathway. The levels of SULTs and ROS may reflect the response manners of ATC cells to resveratrol.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2018/6235417</identifier><identifier>PMID: 30116486</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Acetylcysteine ; Antioxidants ; Antioxidants - pharmacology ; Antioxidants - therapeutic use ; Apoptosis ; Cancer ; Cancer cells ; Cancer therapies ; Care and treatment ; Cell culture ; Cell growth ; Chemotherapy ; Health aspects ; Humans ; Laboratories ; Metabolism ; Mitochondria ; Oxidative stress ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Resveratrol ; Resveratrol - pharmacology ; Resveratrol - therapeutic use ; Superoxide ; T cells ; Thyroid cancer ; Thyroid Carcinoma, Anaplastic - diagnosis ; Thyroid gland</subject><ispartof>Oxidative medicine and cellular longevity, 2018-01, Vol.2018 (2018), p.1-12</ispartof><rights>Copyright © 2018 Xu Zheng et al.</rights><rights>COPYRIGHT 2018 John Wiley & Sons, Inc.</rights><rights>Copyright © 2018 Xu Zheng et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. http://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2018 Xu Zheng et al. 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c499t-ac3de96b52a193ca6d2b64601df45896410a450539a18bc6482e352118163fb3</citedby><cites>FETCH-LOGICAL-c499t-ac3de96b52a193ca6d2b64601df45896410a450539a18bc6482e352118163fb3</cites><orcidid>0000-0002-6866-719X ; 0000-0002-0562-5638</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6079360/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6079360/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30116486$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Crabtree, Mark</contributor><contributor>Mark Crabtree</contributor><creatorcontrib>Liu, Jia</creatorcontrib><creatorcontrib>Kong, Qing-You</creatorcontrib><creatorcontrib>Wu, Mo-Li</creatorcontrib><creatorcontrib>Song, Xue</creatorcontrib><creatorcontrib>Tian, Xiao-Ting</creatorcontrib><creatorcontrib>Jia, Bin</creatorcontrib><creatorcontrib>Zheng, Xu</creatorcontrib><creatorcontrib>Li, Hong</creatorcontrib><title>Correlation of Reactive Oxygen Species Levels with Resveratrol Sensitivities of Anaplastic Thyroid Cancer Cells</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>Anaplastic thyroid carcinoma (ATC) is the most lethal thyroid malignancy without a reliable therapeutic agent. Resveratrol possesses cancer-suppressive effects, while its effect(s) on ATC cells remains unknown. Because oxidative damage caused by increased reactive oxygen species (ROS) is one of the therapeutic effects of anticancer drugs and oxidative stress-caused mitochondria swelling is observed in resveratrol-treated cancer cells, the oxidative statuses and their relevance with resveratrol sensitivities are elucidated using THJ-16T and THJ-11T ATC cells established from two human anaplastic thyroid carcinoma cases. The results revealed that resveratrol-treated THJ-16T rather than THJ-11T cells showed remarkable growth arrest and extensive apoptosis accompanied with the elevated ROS generation and the attenuated superoxide dismutase 2 (SOD2) and catalase (CAT) levels. Mitochondrial impairment and the enhanced caspase-9/caspase-3 activation are found only in resveratrol-sensitive THJ-16T cells. Treatment with the antioxidant N-acetylcysteine (NAC) partly attenuated resveratrol-induced ROS generation and apoptosis of THJ-16T cells. The levels of resveratrol metabolic enzymes (SULT1A1 and SULT1C2) in THJ-16T cells were lower than those in THJ-11T cells and therefore reversely related with resveratrol sensitivities of ATC cells. Our findings demonstrate the ability of resveratrol to increase ROS generation and oxidative-related cellular lesions in resveratrol-sensitive THJ-16T cells presumably through activating the ROS-mitochondrial signal pathway. The levels of SULTs and ROS may reflect the response manners of ATC cells to resveratrol.</description><subject>Acetylcysteine</subject><subject>Antioxidants</subject><subject>Antioxidants - pharmacology</subject><subject>Antioxidants - therapeutic use</subject><subject>Apoptosis</subject><subject>Cancer</subject><subject>Cancer cells</subject><subject>Cancer therapies</subject><subject>Care and treatment</subject><subject>Cell culture</subject><subject>Cell growth</subject><subject>Chemotherapy</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Laboratories</subject><subject>Metabolism</subject><subject>Mitochondria</subject><subject>Oxidative stress</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Resveratrol</subject><subject>Resveratrol - pharmacology</subject><subject>Resveratrol - therapeutic use</subject><subject>Superoxide</subject><subject>T cells</subject><subject>Thyroid cancer</subject><subject>Thyroid Carcinoma, Anaplastic - diagnosis</subject><subject>Thyroid gland</subject><issn>1942-0900</issn><issn>1942-0994</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNkcuLUzEUxoMozljduZaAG0Hr5H2TjVAuvqAw4HQf0txz2wy3SU1uO_a_N6W1PlYuQgLnl--c73wIvaTkPaVS3jBC9Y1iXAraPELX1Ag2JcaIx5c3IVfoWSn3hCjOBH2KrjihVAmtrlFqU84wuDGkiFOPv4HzY9gDvv1xWEHEd1vwAQqewx6Ggh_CuK5M2UN2Y04DvoNYQv1QT6WqwCy67eDKGDxerA85hQ63LnrIuIVhKM_Rk94NBV6c7wlafPq4aL9M57efv7az-dQLY8ap87wDo5aSOWq4d6pjSyUUoV0vpDZKUOKEJJIbR_XSVy8MuGSUaqp4v-QT9OEku90tN9B5iGN2g93msHH5YJML9u9KDGu7SnurSGO4IlXgzVkgp-87KKPdhOKrAxch7YplRBstpa7TTdDrf9D7tMuxuqtUI4jRoi7-Qq3cADbEPtW-_ihqZ4qwhjac6Uq9O1E-p1Iy9JeRKbHHuO0xbnuOu-Kv_rR5gX_lW4G3J2AdYucewn_KQWWgd7_putlGCf4Tbtm7dg</recordid><startdate>20180101</startdate><enddate>20180101</enddate><creator>Liu, Jia</creator><creator>Kong, Qing-You</creator><creator>Wu, Mo-Li</creator><creator>Song, Xue</creator><creator>Tian, Xiao-Ting</creator><creator>Jia, Bin</creator><creator>Zheng, Xu</creator><creator>Li, Hong</creator><general>Hindawi Publishing Corporation</general><general>Hindawi</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-6866-719X</orcidid><orcidid>https://orcid.org/0000-0002-0562-5638</orcidid></search><sort><creationdate>20180101</creationdate><title>Correlation of Reactive Oxygen Species Levels with Resveratrol Sensitivities of Anaplastic Thyroid Cancer Cells</title><author>Liu, Jia ; Kong, Qing-You ; Wu, Mo-Li ; Song, Xue ; Tian, Xiao-Ting ; Jia, Bin ; Zheng, Xu ; Li, Hong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c499t-ac3de96b52a193ca6d2b64601df45896410a450539a18bc6482e352118163fb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Acetylcysteine</topic><topic>Antioxidants</topic><topic>Antioxidants - pharmacology</topic><topic>Antioxidants - therapeutic use</topic><topic>Apoptosis</topic><topic>Cancer</topic><topic>Cancer cells</topic><topic>Cancer therapies</topic><topic>Care and treatment</topic><topic>Cell culture</topic><topic>Cell growth</topic><topic>Chemotherapy</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Laboratories</topic><topic>Metabolism</topic><topic>Mitochondria</topic><topic>Oxidative stress</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Resveratrol</topic><topic>Resveratrol - pharmacology</topic><topic>Resveratrol - therapeutic use</topic><topic>Superoxide</topic><topic>T cells</topic><topic>Thyroid cancer</topic><topic>Thyroid Carcinoma, Anaplastic - diagnosis</topic><topic>Thyroid gland</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Jia</creatorcontrib><creatorcontrib>Kong, Qing-You</creatorcontrib><creatorcontrib>Wu, Mo-Li</creatorcontrib><creatorcontrib>Song, Xue</creatorcontrib><creatorcontrib>Tian, Xiao-Ting</creatorcontrib><creatorcontrib>Jia, Bin</creatorcontrib><creatorcontrib>Zheng, Xu</creatorcontrib><creatorcontrib>Li, Hong</creatorcontrib><collection>الدوريات العلمية والإحصائية - e-Marefa Academic and Statistical Periodicals</collection><collection>معرفة - المحتوى العربي الأكاديمي المتكامل - e-Marefa Academic Complete</collection><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access 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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oxidative medicine and cellular longevity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Jia</au><au>Kong, Qing-You</au><au>Wu, Mo-Li</au><au>Song, Xue</au><au>Tian, Xiao-Ting</au><au>Jia, Bin</au><au>Zheng, Xu</au><au>Li, Hong</au><au>Crabtree, Mark</au><au>Mark Crabtree</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Correlation of Reactive Oxygen Species Levels with Resveratrol Sensitivities of Anaplastic Thyroid Cancer Cells</atitle><jtitle>Oxidative medicine and cellular longevity</jtitle><addtitle>Oxid Med Cell Longev</addtitle><date>2018-01-01</date><risdate>2018</risdate><volume>2018</volume><issue>2018</issue><spage>1</spage><epage>12</epage><pages>1-12</pages><issn>1942-0900</issn><eissn>1942-0994</eissn><abstract>Anaplastic thyroid carcinoma (ATC) is the most lethal thyroid malignancy without a reliable therapeutic agent. Resveratrol possesses cancer-suppressive effects, while its effect(s) on ATC cells remains unknown. Because oxidative damage caused by increased reactive oxygen species (ROS) is one of the therapeutic effects of anticancer drugs and oxidative stress-caused mitochondria swelling is observed in resveratrol-treated cancer cells, the oxidative statuses and their relevance with resveratrol sensitivities are elucidated using THJ-16T and THJ-11T ATC cells established from two human anaplastic thyroid carcinoma cases. The results revealed that resveratrol-treated THJ-16T rather than THJ-11T cells showed remarkable growth arrest and extensive apoptosis accompanied with the elevated ROS generation and the attenuated superoxide dismutase 2 (SOD2) and catalase (CAT) levels. Mitochondrial impairment and the enhanced caspase-9/caspase-3 activation are found only in resveratrol-sensitive THJ-16T cells. Treatment with the antioxidant N-acetylcysteine (NAC) partly attenuated resveratrol-induced ROS generation and apoptosis of THJ-16T cells. The levels of resveratrol metabolic enzymes (SULT1A1 and SULT1C2) in THJ-16T cells were lower than those in THJ-11T cells and therefore reversely related with resveratrol sensitivities of ATC cells. Our findings demonstrate the ability of resveratrol to increase ROS generation and oxidative-related cellular lesions in resveratrol-sensitive THJ-16T cells presumably through activating the ROS-mitochondrial signal pathway. The levels of SULTs and ROS may reflect the response manners of ATC cells to resveratrol.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>30116486</pmid><doi>10.1155/2018/6235417</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-6866-719X</orcidid><orcidid>https://orcid.org/0000-0002-0562-5638</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central Open Access; Wiley Online Library Open Access; PubMed Central; Alma/SFX Local Collection |
| subjects | Acetylcysteine Antioxidants Antioxidants - pharmacology Antioxidants - therapeutic use Apoptosis Cancer Cancer cells Cancer therapies Care and treatment Cell culture Cell growth Chemotherapy Health aspects Humans Laboratories Metabolism Mitochondria Oxidative stress Reactive oxygen species Reactive Oxygen Species - metabolism Resveratrol Resveratrol - pharmacology Resveratrol - therapeutic use Superoxide T cells Thyroid cancer Thyroid Carcinoma, Anaplastic - diagnosis Thyroid gland |
| title | Correlation of Reactive Oxygen Species Levels with Resveratrol Sensitivities of Anaplastic Thyroid Cancer Cells |
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