Exogenous Hydrogen Sulfide Regulates the Growth of Human Thyroid Carcinoma Cells
Hydrogen sulfide (H2S) is involved in the development and progression of many types of cancer. However, the effect and mechanism of H2S on the growth of human thyroid carcinoma cells remain unknown. In the present study, we found that the proliferation, viability, migration, and invasion of human th...
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| Veröffentlicht in: | Oxidative medicine and cellular longevity 2019-01, Vol.2019 (2019), p.1-18 |
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| creator | Li, Yanzhang Ji, Ailing Wang, Huijuan Liu, Zhengguo Zhong, Peiyu Tian, Wenke Zhang, Qianqian Li, Jianmei Wu, Dongdong Wang, Honggang |
| description | Hydrogen sulfide (H2S) is involved in the development and progression of many types of cancer. However, the effect and mechanism of H2S on the growth of human thyroid carcinoma cells remain unknown. In the present study, we found that the proliferation, viability, migration, and invasion of human thyroid carcinoma cells were enhanced by 25–50 μM NaHS (an H2S donor) and inhibited by 200 μM NaHS. However, H2S showed no obvious effects on the proliferation, viability, and migration of human normal thyroid cells. Administration of 50 μM NaHS increased the expression levels of CBS, SQR, and TST, while 200 μM NaHS showed reverse effects in human thyroid carcinoma cells. After treatment with 25-50 μM NaHS, the ROS levels were decreased and the protein levels of p-PI3K, p-AKT, p-mTOR, H-RAS, p-RAF, p-MEK1/2, and p-ERK1/2 were increased, whereas 200 μM NaHS exerted opposite effects in human thyroid carcinoma cells. Furthermore, 1.4-2.8 mg/kg/day NaHS promoted the tumor growth and blood vessel formation in human thyroid carcinoma xenograft tumors, while 11.2 mg/kg/day NaHS inhibited the tumor growth and angiogenesis. In conclusion, our results demonstrate that exogenous H2S regulates the growth of human thyroid carcinoma cells through ROS/PI3K/Akt/mTOR and RAS/RAF/MEK/ERK signaling pathways. Novel H2S-releasing donors/drugs can be designed and applied for the treatment of thyroid cancer. |
| doi_str_mv | 10.1155/2019/6927298 |
| format | Article |
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However, the effect and mechanism of H2S on the growth of human thyroid carcinoma cells remain unknown. In the present study, we found that the proliferation, viability, migration, and invasion of human thyroid carcinoma cells were enhanced by 25–50 μM NaHS (an H2S donor) and inhibited by 200 μM NaHS. However, H2S showed no obvious effects on the proliferation, viability, and migration of human normal thyroid cells. Administration of 50 μM NaHS increased the expression levels of CBS, SQR, and TST, while 200 μM NaHS showed reverse effects in human thyroid carcinoma cells. After treatment with 25-50 μM NaHS, the ROS levels were decreased and the protein levels of p-PI3K, p-AKT, p-mTOR, H-RAS, p-RAF, p-MEK1/2, and p-ERK1/2 were increased, whereas 200 μM NaHS exerted opposite effects in human thyroid carcinoma cells. Furthermore, 1.4-2.8 mg/kg/day NaHS promoted the tumor growth and blood vessel formation in human thyroid carcinoma xenograft tumors, while 11.2 mg/kg/day NaHS inhibited the tumor growth and angiogenesis. In conclusion, our results demonstrate that exogenous H2S regulates the growth of human thyroid carcinoma cells through ROS/PI3K/Akt/mTOR and RAS/RAF/MEK/ERK signaling pathways. Novel H2S-releasing donors/drugs can be designed and applied for the treatment of thyroid cancer.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2019/6927298</identifier><identifier>PMID: 31223424</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Angiogenesis ; Cancer ; Carcinoma ; Cell adhesion & migration ; Cell growth ; Cell Line, Tumor ; Cell Proliferation ; Development and progression ; Enzymes ; Growth ; Humans ; Hydrogen sulfide ; Hydrogen Sulfide - metabolism ; Kinases ; Medical research ; Neovascularization ; Stem cells ; Sulfur ; Thyroid cancer ; Thyroid gland ; Thyroid Neoplasms - metabolism ; Tumors</subject><ispartof>Oxidative medicine and cellular longevity, 2019-01, Vol.2019 (2019), p.1-18</ispartof><rights>Copyright © 2019 Dongdong Wu et al.</rights><rights>COPYRIGHT 2019 John Wiley & Sons, Inc.</rights><rights>Copyright © 2019 Dongdong Wu 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 © 2019 Dongdong Wu et al. 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c499t-ba79c81c39eb09d48df6470e3b72811fe5bc04936b6f57221530851a4bb68c803</citedby><cites>FETCH-LOGICAL-c499t-ba79c81c39eb09d48df6470e3b72811fe5bc04936b6f57221530851a4bb68c803</cites><orcidid>0000-0002-7327-0015 ; 0000-0001-6739-8437 ; 0000-0003-0166-5226</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/PMC6541980/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6541980/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31223424$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Giustarini, Daniela</contributor><contributor>Daniela Giustarini</contributor><creatorcontrib>Li, Yanzhang</creatorcontrib><creatorcontrib>Ji, Ailing</creatorcontrib><creatorcontrib>Wang, Huijuan</creatorcontrib><creatorcontrib>Liu, Zhengguo</creatorcontrib><creatorcontrib>Zhong, Peiyu</creatorcontrib><creatorcontrib>Tian, Wenke</creatorcontrib><creatorcontrib>Zhang, Qianqian</creatorcontrib><creatorcontrib>Li, Jianmei</creatorcontrib><creatorcontrib>Wu, Dongdong</creatorcontrib><creatorcontrib>Wang, Honggang</creatorcontrib><title>Exogenous Hydrogen Sulfide Regulates the Growth of Human Thyroid Carcinoma Cells</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>Hydrogen sulfide (H2S) is involved in the development and progression of many types of cancer. However, the effect and mechanism of H2S on the growth of human thyroid carcinoma cells remain unknown. In the present study, we found that the proliferation, viability, migration, and invasion of human thyroid carcinoma cells were enhanced by 25–50 μM NaHS (an H2S donor) and inhibited by 200 μM NaHS. However, H2S showed no obvious effects on the proliferation, viability, and migration of human normal thyroid cells. Administration of 50 μM NaHS increased the expression levels of CBS, SQR, and TST, while 200 μM NaHS showed reverse effects in human thyroid carcinoma cells. After treatment with 25-50 μM NaHS, the ROS levels were decreased and the protein levels of p-PI3K, p-AKT, p-mTOR, H-RAS, p-RAF, p-MEK1/2, and p-ERK1/2 were increased, whereas 200 μM NaHS exerted opposite effects in human thyroid carcinoma cells. Furthermore, 1.4-2.8 mg/kg/day NaHS promoted the tumor growth and blood vessel formation in human thyroid carcinoma xenograft tumors, while 11.2 mg/kg/day NaHS inhibited the tumor growth and angiogenesis. In conclusion, our results demonstrate that exogenous H2S regulates the growth of human thyroid carcinoma cells through ROS/PI3K/Akt/mTOR and RAS/RAF/MEK/ERK signaling pathways. Novel H2S-releasing donors/drugs can be designed and applied for the treatment of thyroid cancer.</description><subject>Angiogenesis</subject><subject>Cancer</subject><subject>Carcinoma</subject><subject>Cell adhesion & migration</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Development and progression</subject><subject>Enzymes</subject><subject>Growth</subject><subject>Humans</subject><subject>Hydrogen sulfide</subject><subject>Hydrogen Sulfide - metabolism</subject><subject>Kinases</subject><subject>Medical research</subject><subject>Neovascularization</subject><subject>Stem cells</subject><subject>Sulfur</subject><subject>Thyroid cancer</subject><subject>Thyroid gland</subject><subject>Thyroid Neoplasms - metabolism</subject><subject>Tumors</subject><issn>1942-0900</issn><issn>1942-0994</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNkd1rFDEUxYMo9kPffJaAL0Jdm5tkMpMXoSy1KxQUrc8hk0l2UmaSmsxY9783665b9cmnXMiPc-85B6EXQN4CVNU5JSDPhaQ1lc0jdAyS0wWRkj8-zIQcoZOcbwkRjHJ4io4YUMo45cfo0-WPuLYhzhmvNl3azvjLPDjfWfzZrudBTzbjqbf4KsX7qcfR4dU86oBv-k2KvsNLnYwPcdR4aYchP0NPnB6yfb5_T9HX95c3y9Xi-uPVh-XF9cJwKadFq2tpGjBM2pbIjjedE7wmlrU1bQCcrVpDuGSiFa6qKYWKkaYCzdtWNKYh7BS92-neze1oO2PDlPSg7pIfddqoqL36-yf4Xq3jdyUqDvKXwOu9QIrfZpsnNfpsigUdbIlDUcorQQkHXtBX_6C3cU6h2CsUIyVTIeQDtdaDVT64WPaarai6EMBqECX_Qr3ZUSbFnJN1h5OBqG2haluo2hda8Jd_2jzAvxsswNkO6H3o9L3_TzlbGOv0A12cSgD2E5jusAQ</recordid><startdate>20190101</startdate><enddate>20190101</enddate><creator>Li, Yanzhang</creator><creator>Ji, Ailing</creator><creator>Wang, Huijuan</creator><creator>Liu, Zhengguo</creator><creator>Zhong, Peiyu</creator><creator>Tian, Wenke</creator><creator>Zhang, Qianqian</creator><creator>Li, Jianmei</creator><creator>Wu, Dongdong</creator><creator>Wang, Honggang</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/0000-0002-7327-0015</orcidid><orcidid>https://orcid.org/0000-0001-6739-8437</orcidid><orcidid>https://orcid.org/0000-0003-0166-5226</orcidid></search><sort><creationdate>20190101</creationdate><title>Exogenous Hydrogen Sulfide Regulates the Growth of Human Thyroid Carcinoma Cells</title><author>Li, Yanzhang ; Ji, Ailing ; Wang, Huijuan ; Liu, Zhengguo ; Zhong, Peiyu ; Tian, Wenke ; Zhang, Qianqian ; Li, Jianmei ; Wu, Dongdong ; Wang, Honggang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c499t-ba79c81c39eb09d48df6470e3b72811fe5bc04936b6f57221530851a4bb68c803</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Angiogenesis</topic><topic>Cancer</topic><topic>Carcinoma</topic><topic>Cell adhesion & migration</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Development and progression</topic><topic>Enzymes</topic><topic>Growth</topic><topic>Humans</topic><topic>Hydrogen sulfide</topic><topic>Hydrogen Sulfide - metabolism</topic><topic>Kinases</topic><topic>Medical research</topic><topic>Neovascularization</topic><topic>Stem cells</topic><topic>Sulfur</topic><topic>Thyroid cancer</topic><topic>Thyroid gland</topic><topic>Thyroid Neoplasms - metabolism</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Yanzhang</creatorcontrib><creatorcontrib>Ji, Ailing</creatorcontrib><creatorcontrib>Wang, Huijuan</creatorcontrib><creatorcontrib>Liu, Zhengguo</creatorcontrib><creatorcontrib>Zhong, Peiyu</creatorcontrib><creatorcontrib>Tian, Wenke</creatorcontrib><creatorcontrib>Zhang, Qianqian</creatorcontrib><creatorcontrib>Li, Jianmei</creatorcontrib><creatorcontrib>Wu, Dongdong</creatorcontrib><creatorcontrib>Wang, Honggang</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</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>Li, Yanzhang</au><au>Ji, Ailing</au><au>Wang, Huijuan</au><au>Liu, Zhengguo</au><au>Zhong, Peiyu</au><au>Tian, Wenke</au><au>Zhang, Qianqian</au><au>Li, Jianmei</au><au>Wu, Dongdong</au><au>Wang, Honggang</au><au>Giustarini, Daniela</au><au>Daniela Giustarini</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Exogenous Hydrogen Sulfide Regulates the Growth of Human Thyroid Carcinoma Cells</atitle><jtitle>Oxidative medicine and cellular longevity</jtitle><addtitle>Oxid Med Cell Longev</addtitle><date>2019-01-01</date><risdate>2019</risdate><volume>2019</volume><issue>2019</issue><spage>1</spage><epage>18</epage><pages>1-18</pages><issn>1942-0900</issn><eissn>1942-0994</eissn><abstract>Hydrogen sulfide (H2S) is involved in the development and progression of many types of cancer. However, the effect and mechanism of H2S on the growth of human thyroid carcinoma cells remain unknown. In the present study, we found that the proliferation, viability, migration, and invasion of human thyroid carcinoma cells were enhanced by 25–50 μM NaHS (an H2S donor) and inhibited by 200 μM NaHS. However, H2S showed no obvious effects on the proliferation, viability, and migration of human normal thyroid cells. Administration of 50 μM NaHS increased the expression levels of CBS, SQR, and TST, while 200 μM NaHS showed reverse effects in human thyroid carcinoma cells. After treatment with 25-50 μM NaHS, the ROS levels were decreased and the protein levels of p-PI3K, p-AKT, p-mTOR, H-RAS, p-RAF, p-MEK1/2, and p-ERK1/2 were increased, whereas 200 μM NaHS exerted opposite effects in human thyroid carcinoma cells. Furthermore, 1.4-2.8 mg/kg/day NaHS promoted the tumor growth and blood vessel formation in human thyroid carcinoma xenograft tumors, while 11.2 mg/kg/day NaHS inhibited the tumor growth and angiogenesis. In conclusion, our results demonstrate that exogenous H2S regulates the growth of human thyroid carcinoma cells through ROS/PI3K/Akt/mTOR and RAS/RAF/MEK/ERK signaling pathways. Novel H2S-releasing donors/drugs can be designed and applied for the treatment of thyroid cancer.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>31223424</pmid><doi>10.1155/2019/6927298</doi><tpages>18</tpages><orcidid>https://orcid.org/0000-0002-7327-0015</orcidid><orcidid>https://orcid.org/0000-0001-6739-8437</orcidid><orcidid>https://orcid.org/0000-0003-0166-5226</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Angiogenesis Cancer Carcinoma Cell adhesion & migration Cell growth Cell Line, Tumor Cell Proliferation Development and progression Enzymes Growth Humans Hydrogen sulfide Hydrogen Sulfide - metabolism Kinases Medical research Neovascularization Stem cells Sulfur Thyroid cancer Thyroid gland Thyroid Neoplasms - metabolism Tumors |
| title | Exogenous Hydrogen Sulfide Regulates the Growth of Human Thyroid Carcinoma Cells |
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