Cantharidin decreased viable cell number in human osteosarcoma U-2 OS cells through G2/M phase arrest and induction of cell apoptosis
Cantharidin (CTD), a sesquiterpenoid bioactive substance, has been reported to exhibit anticancer activity against various types of cancer cells. The aim of the present study was to investigate the apoptosis effects and the underlying mechanisms of CTD on osteosarcoma U-2 OS cells. Results showed th...
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| Veröffentlicht in: | Bioscience, biotechnology, and biochemistry biotechnology, and biochemistry, 2019-10, Vol.83 (10), p.1912-1923 |
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| container_title | Bioscience, biotechnology, and biochemistry |
| container_volume | 83 |
| creator | Chen, Chia-Ching Chueh, Fu-Shin Peng, Shu-Fen Huang, Wen-Wen Tsai, Chang-Hai Tsai, Fuu-Jen Huang, Chih-Yang Tang, Chih-Hsin Yang, Jai-Sing Hsu, Yuan-Man Yin, Mei-Chin Huang, Yi-Ping Chung, Jing-Gung |
| description | Cantharidin (CTD), a sesquiterpenoid bioactive substance, has been reported to exhibit anticancer activity against various types of cancer cells. The aim of the present study was to investigate the apoptosis effects and the underlying mechanisms of CTD on osteosarcoma U-2 OS cells. Results showed that CTD induced cell morphologic changes, reduced total viable cells, induced DNA damage, and G
2
/M phase arrest. CTD increased the production of reactive oxygen species and Ca
2+
, and elevated the activities of caspase-3 and −9, but decreased the level of mitochondrial membrane potential. Furthermore, CTD increased the ROS- and ER stress-associated protein expressions and increased the levels of pro-apoptosis-associated proteins, but decreased that of anti-apoptosis-associated proteins. Based on these observations, we suggested that CTD decreased cell number through G
2
/M phase arrest and the induction of cell apoptosis in U-2 OS cells and CTD could be a potential candidate for osteosarcoma treatments.
The possible signaling pathways for CTD induced apoptosis in U-2 OS human osteosarcoma cancer cells |
| doi_str_mv | 10.1080/09168451.2019.1627182 |
| format | Article |
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2
/M phase arrest. CTD increased the production of reactive oxygen species and Ca
2+
, and elevated the activities of caspase-3 and −9, but decreased the level of mitochondrial membrane potential. Furthermore, CTD increased the ROS- and ER stress-associated protein expressions and increased the levels of pro-apoptosis-associated proteins, but decreased that of anti-apoptosis-associated proteins. Based on these observations, we suggested that CTD decreased cell number through G
2
/M phase arrest and the induction of cell apoptosis in U-2 OS cells and CTD could be a potential candidate for osteosarcoma treatments.
The possible signaling pathways for CTD induced apoptosis in U-2 OS human osteosarcoma cancer cells</description><identifier>ISSN: 0916-8451</identifier><identifier>EISSN: 1347-6947</identifier><identifier>DOI: 10.1080/09168451.2019.1627182</identifier><language>eng</language><publisher>Taylor & Francis</publisher><subject>apoptosis ; Cantharidin ; cell cycle ; M phase arrest ; osteosarcoma U-2 OS cells</subject><ispartof>Bioscience, biotechnology, and biochemistry, 2019-10, Vol.83 (10), p.1912-1923</ispartof><rights>2019 Japan Society for Bioscience, Biotechnology, and Agrochemistry 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3702-2cfdbe9ffb0f71281f5ba9f677103e193e52ad023f3f2aadd481386c81ba4a503</citedby><cites>FETCH-LOGICAL-c3702-2cfdbe9ffb0f71281f5ba9f677103e193e52ad023f3f2aadd481386c81ba4a503</cites><orcidid>0000-0002-4575-7475</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27926,27927</link.rule.ids></links><search><creatorcontrib>Chen, Chia-Ching</creatorcontrib><creatorcontrib>Chueh, Fu-Shin</creatorcontrib><creatorcontrib>Peng, Shu-Fen</creatorcontrib><creatorcontrib>Huang, Wen-Wen</creatorcontrib><creatorcontrib>Tsai, Chang-Hai</creatorcontrib><creatorcontrib>Tsai, Fuu-Jen</creatorcontrib><creatorcontrib>Huang, Chih-Yang</creatorcontrib><creatorcontrib>Tang, Chih-Hsin</creatorcontrib><creatorcontrib>Yang, Jai-Sing</creatorcontrib><creatorcontrib>Hsu, Yuan-Man</creatorcontrib><creatorcontrib>Yin, Mei-Chin</creatorcontrib><creatorcontrib>Huang, Yi-Ping</creatorcontrib><creatorcontrib>Chung, Jing-Gung</creatorcontrib><title>Cantharidin decreased viable cell number in human osteosarcoma U-2 OS cells through G2/M phase arrest and induction of cell apoptosis</title><title>Bioscience, biotechnology, and biochemistry</title><description>Cantharidin (CTD), a sesquiterpenoid bioactive substance, has been reported to exhibit anticancer activity against various types of cancer cells. The aim of the present study was to investigate the apoptosis effects and the underlying mechanisms of CTD on osteosarcoma U-2 OS cells. Results showed that CTD induced cell morphologic changes, reduced total viable cells, induced DNA damage, and G
2
/M phase arrest. CTD increased the production of reactive oxygen species and Ca
2+
, and elevated the activities of caspase-3 and −9, but decreased the level of mitochondrial membrane potential. Furthermore, CTD increased the ROS- and ER stress-associated protein expressions and increased the levels of pro-apoptosis-associated proteins, but decreased that of anti-apoptosis-associated proteins. Based on these observations, we suggested that CTD decreased cell number through G
2
/M phase arrest and the induction of cell apoptosis in U-2 OS cells and CTD could be a potential candidate for osteosarcoma treatments.
The possible signaling pathways for CTD induced apoptosis in U-2 OS human osteosarcoma cancer cells</description><subject>apoptosis</subject><subject>Cantharidin</subject><subject>cell cycle</subject><subject>M phase arrest</subject><subject>osteosarcoma U-2 OS cells</subject><issn>0916-8451</issn><issn>1347-6947</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNqNkMtO3TAQhi1EJQ60j1DJy25y8Ni5OLuiIwqVQCxa1tbEF2KUxMFOqHgA3pukoduK1Ugz3_9p9BPyFdgemGTnrIZS5gXsOYN6DyWvQPIjsgORV1lZ59Ux2a1MtkIn5DSlR8aWRQE78nrAYWoxeuMHaqyOFpM19Nlj01mqbdfRYe4bG-lyb-ceBxrSZEPCqEOP9D7j9O7XXzDRqY1hfmjpFT-_pWO7mCjGaNNEcTCLwMx68mExuM2MYxinkHz6TD457JL98j7PyP2Py9-H6-zm7urn4eIm06JiPOPamcbWzjXMVcAluKLB2pVVBUxYqIUtOBrGhROOIxqTSxCy1BIazLFg4ox827xjDE_z8pjqfVpfwcGGOSnOJS-AVbJe0GJDdQwpRevUGH2P8UUBU2vt6l_taq1dvde-5NiWC_P44cj3LeIHF2KPf0LsjJrwpQvRRRy0T0r8X_EG1eWYUA</recordid><startdate>20191003</startdate><enddate>20191003</enddate><creator>Chen, Chia-Ching</creator><creator>Chueh, Fu-Shin</creator><creator>Peng, Shu-Fen</creator><creator>Huang, Wen-Wen</creator><creator>Tsai, Chang-Hai</creator><creator>Tsai, Fuu-Jen</creator><creator>Huang, Chih-Yang</creator><creator>Tang, Chih-Hsin</creator><creator>Yang, Jai-Sing</creator><creator>Hsu, Yuan-Man</creator><creator>Yin, Mei-Chin</creator><creator>Huang, Yi-Ping</creator><creator>Chung, Jing-Gung</creator><general>Taylor & Francis</general><general>Oxford University Press</general><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-4575-7475</orcidid></search><sort><creationdate>20191003</creationdate><title>Cantharidin decreased viable cell number in human osteosarcoma U-2 OS cells through G2/M phase arrest and induction of cell apoptosis</title><author>Chen, Chia-Ching ; Chueh, Fu-Shin ; Peng, Shu-Fen ; Huang, Wen-Wen ; Tsai, Chang-Hai ; Tsai, Fuu-Jen ; Huang, Chih-Yang ; Tang, Chih-Hsin ; Yang, Jai-Sing ; Hsu, Yuan-Man ; Yin, Mei-Chin ; Huang, Yi-Ping ; Chung, Jing-Gung</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3702-2cfdbe9ffb0f71281f5ba9f677103e193e52ad023f3f2aadd481386c81ba4a503</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>apoptosis</topic><topic>Cantharidin</topic><topic>cell cycle</topic><topic>M phase arrest</topic><topic>osteosarcoma U-2 OS cells</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Chia-Ching</creatorcontrib><creatorcontrib>Chueh, Fu-Shin</creatorcontrib><creatorcontrib>Peng, Shu-Fen</creatorcontrib><creatorcontrib>Huang, Wen-Wen</creatorcontrib><creatorcontrib>Tsai, Chang-Hai</creatorcontrib><creatorcontrib>Tsai, Fuu-Jen</creatorcontrib><creatorcontrib>Huang, Chih-Yang</creatorcontrib><creatorcontrib>Tang, Chih-Hsin</creatorcontrib><creatorcontrib>Yang, Jai-Sing</creatorcontrib><creatorcontrib>Hsu, Yuan-Man</creatorcontrib><creatorcontrib>Yin, Mei-Chin</creatorcontrib><creatorcontrib>Huang, Yi-Ping</creatorcontrib><creatorcontrib>Chung, Jing-Gung</creatorcontrib><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Bioscience, biotechnology, and biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Chia-Ching</au><au>Chueh, Fu-Shin</au><au>Peng, Shu-Fen</au><au>Huang, Wen-Wen</au><au>Tsai, Chang-Hai</au><au>Tsai, Fuu-Jen</au><au>Huang, Chih-Yang</au><au>Tang, Chih-Hsin</au><au>Yang, Jai-Sing</au><au>Hsu, Yuan-Man</au><au>Yin, Mei-Chin</au><au>Huang, Yi-Ping</au><au>Chung, Jing-Gung</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cantharidin decreased viable cell number in human osteosarcoma U-2 OS cells through G2/M phase arrest and induction of cell apoptosis</atitle><jtitle>Bioscience, biotechnology, and biochemistry</jtitle><date>2019-10-03</date><risdate>2019</risdate><volume>83</volume><issue>10</issue><spage>1912</spage><epage>1923</epage><pages>1912-1923</pages><issn>0916-8451</issn><eissn>1347-6947</eissn><abstract>Cantharidin (CTD), a sesquiterpenoid bioactive substance, has been reported to exhibit anticancer activity against various types of cancer cells. The aim of the present study was to investigate the apoptosis effects and the underlying mechanisms of CTD on osteosarcoma U-2 OS cells. Results showed that CTD induced cell morphologic changes, reduced total viable cells, induced DNA damage, and G
2
/M phase arrest. CTD increased the production of reactive oxygen species and Ca
2+
, and elevated the activities of caspase-3 and −9, but decreased the level of mitochondrial membrane potential. Furthermore, CTD increased the ROS- and ER stress-associated protein expressions and increased the levels of pro-apoptosis-associated proteins, but decreased that of anti-apoptosis-associated proteins. Based on these observations, we suggested that CTD decreased cell number through G
2
/M phase arrest and the induction of cell apoptosis in U-2 OS cells and CTD could be a potential candidate for osteosarcoma treatments.
The possible signaling pathways for CTD induced apoptosis in U-2 OS human osteosarcoma cancer cells</abstract><pub>Taylor & Francis</pub><doi>10.1080/09168451.2019.1627182</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-4575-7475</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Bioscience, biotechnology, and biochemistry, 2019-10, Vol.83 (10), p.1912-1923 |
| issn | 0916-8451 1347-6947 |
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| source | Oxford University Press Journals All Titles (1996-Current); Open Access Titles of Japan; EZB-FREE-00999 freely available EZB journals |
| subjects | apoptosis Cantharidin cell cycle M phase arrest osteosarcoma U-2 OS cells |
| title | Cantharidin decreased viable cell number in human osteosarcoma U-2 OS cells through G2/M phase arrest and induction of cell apoptosis |
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