Reactive oxygen species generation is essential for cisplatininduced accelerated senescence in hepatocellular carcinoma
Accelerated senescence is important because this process is involved in tumor suppression and has been induced by many chemotherapeutic agents. The platinum-based chemotherapeutic agent cisplatin displays a wide range of antitumor activities. However, the molecular mechanism of cisplatin-induced acc...
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| Veröffentlicht in: | Frontiers of medicine 2014-06, Vol.8 (2), p.227-235 |
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| creator | Qu, Kai Lin, Ting Wang, Zhixin Liu, Sinan Chang, Hulin Xu, Xinsen Meng, Fandi Zhou, Lei Wei, Jichao Tai, Minghui Dong, Yafeng Liu, Chang |
| description | Accelerated senescence is important because this process is involved in tumor suppression and has been induced by many chemotherapeutic agents. The platinum-based chemotherapeutic agent cisplatin displays a wide range of antitumor activities. However, the molecular mechanism of cisplatin-induced accelerated senescence in hepatocellular carcinoma （HCC） remains unclear. In the present study, the growth inhibitory effect of cisplatin on HepG2 and SMMC-7721 cells was detected by 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide assay. Cellular senescence was then assessed by I~-galactosidase assay. Senescence-related factors, including p53, p21, and p16, were evaluated by quantitative reverse transcription-polymerase chain reaction. Reactive oxygen species （ROS） was analyzed by flow cytometry. Our results revealed that cisplatin reduced the proliferation of HepG2 and SMMC-7721 cells in a dose- and time-dependent manner. Senescent phenotype observed in cisplatin- treated hepatoma cells was dependent on p53 and p21 activation but not on pl 6 activation. Furthermore, cisplatininduced accelerated senescence depended on intracellular ROS generation. The ROS scavenger N-acetyl-Lcysteine also significantly suppressed the cisplatin-induced senescence of HepG2 and SMMC-7721 cells. In conclusion, our results revealed a functional link between intracellular ROS generation and cisplatin-indnced accelerated senescence, and this link may be used as a potential target of HCC. |
| doi_str_mv | 10.1007/s11684-014-0327-1 |
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The platinum-based chemotherapeutic agent cisplatin displays a wide range of antitumor activities. However, the molecular mechanism of cisplatin-induced accelerated senescence in hepatocellular carcinoma （HCC） remains unclear. In the present study, the growth inhibitory effect of cisplatin on HepG2 and SMMC-7721 cells was detected by 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide assay. Cellular senescence was then assessed by I~-galactosidase assay. Senescence-related factors, including p53, p21, and p16, were evaluated by quantitative reverse transcription-polymerase chain reaction. Reactive oxygen species （ROS） was analyzed by flow cytometry. Our results revealed that cisplatin reduced the proliferation of HepG2 and SMMC-7721 cells in a dose- and time-dependent manner. Senescent phenotype observed in cisplatin- treated hepatoma cells was dependent on p53 and p21 activation but not on pl 6 activation. Furthermore, cisplatininduced accelerated senescence depended on intracellular ROS generation. The ROS scavenger N-acetyl-Lcysteine also significantly suppressed the cisplatin-induced senescence of HepG2 and SMMC-7721 cells. In conclusion, our results revealed a functional link between intracellular ROS generation and cisplatin-indnced accelerated senescence, and this link may be used as a potential target of HCC.</description><identifier>ISSN: 2095-0217</identifier><identifier>EISSN: 2095-0225</identifier><identifier>DOI: 10.1007/s11684-014-0327-1</identifier><language>eng</language><publisher>Heidelberg: Higher Education Press</publisher><subject>HepG2 ; Liver cancer ; Medicine ; Medicine & Public Health ; p21基因 ; p53基因 ; Reactive oxygen species ; Research Article ; Senescence ; SMMC-7721细胞 ; 活性氧清除剂 ; 细胞衰老 ; 聚合酶链式反应 ; 肝癌细胞</subject><ispartof>Frontiers of medicine, 2014-06, Vol.8 (2), p.227-235</ispartof><rights>Higher Education Press and Springer-Verlag Berlin Heidelberg 2014</rights><rights>Frontiers of Medicine is a copyright of Springer, 2014.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c2571-ad3cc6e4b3468c13412604f10c8bae6700d501b941cea48c3c7e85eb2906fcf53</citedby><cites>FETCH-LOGICAL-c2571-ad3cc6e4b3468c13412604f10c8bae6700d501b941cea48c3c7e85eb2906fcf53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://image.cqvip.com/vip1000/qk/71235X/71235X.jpg</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11684-014-0327-1$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11684-014-0327-1$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids></links><search><creatorcontrib>Qu, Kai</creatorcontrib><creatorcontrib>Lin, Ting</creatorcontrib><creatorcontrib>Wang, Zhixin</creatorcontrib><creatorcontrib>Liu, Sinan</creatorcontrib><creatorcontrib>Chang, Hulin</creatorcontrib><creatorcontrib>Xu, Xinsen</creatorcontrib><creatorcontrib>Meng, Fandi</creatorcontrib><creatorcontrib>Zhou, Lei</creatorcontrib><creatorcontrib>Wei, Jichao</creatorcontrib><creatorcontrib>Tai, Minghui</creatorcontrib><creatorcontrib>Dong, Yafeng</creatorcontrib><creatorcontrib>Liu, Chang</creatorcontrib><title>Reactive oxygen species generation is essential for cisplatininduced accelerated senescence in hepatocellular carcinoma</title><title>Frontiers of medicine</title><addtitle>Front. Med</addtitle><addtitle>Frontiers of Medicine</addtitle><description>Accelerated senescence is important because this process is involved in tumor suppression and has been induced by many chemotherapeutic agents. The platinum-based chemotherapeutic agent cisplatin displays a wide range of antitumor activities. However, the molecular mechanism of cisplatin-induced accelerated senescence in hepatocellular carcinoma （HCC） remains unclear. In the present study, the growth inhibitory effect of cisplatin on HepG2 and SMMC-7721 cells was detected by 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide assay. Cellular senescence was then assessed by I~-galactosidase assay. Senescence-related factors, including p53, p21, and p16, were evaluated by quantitative reverse transcription-polymerase chain reaction. Reactive oxygen species （ROS） was analyzed by flow cytometry. Our results revealed that cisplatin reduced the proliferation of HepG2 and SMMC-7721 cells in a dose- and time-dependent manner. Senescent phenotype observed in cisplatin- treated hepatoma cells was dependent on p53 and p21 activation but not on pl 6 activation. Furthermore, cisplatininduced accelerated senescence depended on intracellular ROS generation. The ROS scavenger N-acetyl-Lcysteine also significantly suppressed the cisplatin-induced senescence of HepG2 and SMMC-7721 cells. In conclusion, our results revealed a functional link between intracellular ROS generation and cisplatin-indnced accelerated senescence, and this link may be used as a potential target of HCC.</description><subject>HepG2</subject><subject>Liver cancer</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>p21基因</subject><subject>p53基因</subject><subject>Reactive oxygen species</subject><subject>Research Article</subject><subject>Senescence</subject><subject>SMMC-7721细胞</subject><subject>活性氧清除剂</subject><subject>细胞衰老</subject><subject>聚合酶链式反应</subject><subject>肝癌细胞</subject><issn>2095-0217</issn><issn>2095-0225</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNp9kFtLxDAQhYsoKOoP8C3iczWTJr08ingDQRB9Dul0upulm3STrpd_b5aK-GRgyIE53xw4WXYG_BI4r64iQFnLnEOaQlQ57GVHgjcq50Ko_V8N1WF2GuOKpydLqJrmKPt4IYOTfSfmP78W5FgcCS1FljQFM1nvmI2MYiQ3WTOw3geGNo5D2jnrui1SxwwiDTt70slIEckhMevYkkYz-bQdtoNJpAlonV-bk-ygN0Ok05__OHu7u329ecifnu8fb66fchSqgtx0BWJJsi1kWSMUEkTJZQ8c69ZQWXHeKQ5tIwHJyBoLrKhW1IqGlz32qjjOLua7Y_CbLcVJr_w2uBSpIVGqLmslkwtmFwYfY6Bej8GuTfjSwPWuYj1XrFPFelexhsSImYnJ6xYU_lz-Bzr_CVp6t9gk7jdJcd40tRTFN-tCi9g</recordid><startdate>20140601</startdate><enddate>20140601</enddate><creator>Qu, Kai</creator><creator>Lin, Ting</creator><creator>Wang, Zhixin</creator><creator>Liu, Sinan</creator><creator>Chang, Hulin</creator><creator>Xu, Xinsen</creator><creator>Meng, Fandi</creator><creator>Zhou, Lei</creator><creator>Wei, Jichao</creator><creator>Tai, Minghui</creator><creator>Dong, Yafeng</creator><creator>Liu, Chang</creator><general>Higher Education Press</general><general>Springer Nature B.V</general><scope>2RA</scope><scope>92L</scope><scope>CQIGP</scope><scope>W91</scope><scope>~WA</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>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20140601</creationdate><title>Reactive oxygen species generation is essential for cisplatininduced accelerated senescence in hepatocellular carcinoma</title><author>Qu, Kai ; Lin, Ting ; Wang, Zhixin ; Liu, Sinan ; Chang, Hulin ; Xu, Xinsen ; Meng, Fandi ; Zhou, Lei ; Wei, Jichao ; Tai, Minghui ; Dong, Yafeng ; Liu, Chang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2571-ad3cc6e4b3468c13412604f10c8bae6700d501b941cea48c3c7e85eb2906fcf53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>HepG2</topic><topic>Liver cancer</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>p21基因</topic><topic>p53基因</topic><topic>Reactive oxygen species</topic><topic>Research Article</topic><topic>Senescence</topic><topic>SMMC-7721细胞</topic><topic>活性氧清除剂</topic><topic>细胞衰老</topic><topic>聚合酶链式反应</topic><topic>肝癌细胞</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Qu, Kai</creatorcontrib><creatorcontrib>Lin, Ting</creatorcontrib><creatorcontrib>Wang, Zhixin</creatorcontrib><creatorcontrib>Liu, Sinan</creatorcontrib><creatorcontrib>Chang, Hulin</creatorcontrib><creatorcontrib>Xu, Xinsen</creatorcontrib><creatorcontrib>Meng, Fandi</creatorcontrib><creatorcontrib>Zhou, Lei</creatorcontrib><creatorcontrib>Wei, Jichao</creatorcontrib><creatorcontrib>Tai, Minghui</creatorcontrib><creatorcontrib>Dong, Yafeng</creatorcontrib><creatorcontrib>Liu, Chang</creatorcontrib><collection>中文科技期刊数据库</collection><collection>中文科技期刊数据库-CALIS站点</collection><collection>中文科技期刊数据库-7.0平台</collection><collection>中文科技期刊数据库-医药卫生</collection><collection>中文科技期刊数据库- 镜像站点</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>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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><jtitle>Frontiers of medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Qu, Kai</au><au>Lin, Ting</au><au>Wang, Zhixin</au><au>Liu, Sinan</au><au>Chang, Hulin</au><au>Xu, Xinsen</au><au>Meng, Fandi</au><au>Zhou, Lei</au><au>Wei, Jichao</au><au>Tai, Minghui</au><au>Dong, Yafeng</au><au>Liu, Chang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reactive oxygen species generation is essential for cisplatininduced accelerated senescence in hepatocellular carcinoma</atitle><jtitle>Frontiers of medicine</jtitle><stitle>Front. Med</stitle><addtitle>Frontiers of Medicine</addtitle><date>2014-06-01</date><risdate>2014</risdate><volume>8</volume><issue>2</issue><spage>227</spage><epage>235</epage><pages>227-235</pages><issn>2095-0217</issn><eissn>2095-0225</eissn><abstract>Accelerated senescence is important because this process is involved in tumor suppression and has been induced by many chemotherapeutic agents. The platinum-based chemotherapeutic agent cisplatin displays a wide range of antitumor activities. However, the molecular mechanism of cisplatin-induced accelerated senescence in hepatocellular carcinoma （HCC） remains unclear. In the present study, the growth inhibitory effect of cisplatin on HepG2 and SMMC-7721 cells was detected by 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide assay. Cellular senescence was then assessed by I~-galactosidase assay. Senescence-related factors, including p53, p21, and p16, were evaluated by quantitative reverse transcription-polymerase chain reaction. Reactive oxygen species （ROS） was analyzed by flow cytometry. Our results revealed that cisplatin reduced the proliferation of HepG2 and SMMC-7721 cells in a dose- and time-dependent manner. Senescent phenotype observed in cisplatin- treated hepatoma cells was dependent on p53 and p21 activation but not on pl 6 activation. Furthermore, cisplatininduced accelerated senescence depended on intracellular ROS generation. The ROS scavenger N-acetyl-Lcysteine also significantly suppressed the cisplatin-induced senescence of HepG2 and SMMC-7721 cells. In conclusion, our results revealed a functional link between intracellular ROS generation and cisplatin-indnced accelerated senescence, and this link may be used as a potential target of HCC.</abstract><cop>Heidelberg</cop><pub>Higher Education Press</pub><doi>10.1007/s11684-014-0327-1</doi><tpages>9</tpages></addata></record> |
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| subjects | HepG2 Liver cancer Medicine Medicine & Public Health p21基因 p53基因 Reactive oxygen species Research Article Senescence SMMC-7721细胞 活性氧清除剂 细胞衰老 聚合酶链式反应 肝癌细胞 |
| title | Reactive oxygen species generation is essential for cisplatininduced accelerated senescence in hepatocellular carcinoma |
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