Inhibitory Effect of Selenium on Esophagus Cancer Cells and the Related Mechanism
Selenium has been associated with many malignant tumors including esophagus cancer (EC). In current study, we examined the effects of three types of selenium, sodium selenite (SSE), methylseleninic acid (MSA) and methylselenocysteine (MSC) on EC cell line Eca109. Here, selenium attenuated cell viabi...
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Veröffentlicht in: | Journal of Nutritional Science and Vitaminology 2020/10/31, Vol.66(5), pp.456-461 |
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description | Selenium has been associated with many malignant tumors including esophagus cancer (EC). In current study, we examined the effects of three types of selenium, sodium selenite (SSE), methylseleninic acid (MSA) and methylselenocysteine (MSC) on EC cell line Eca109. Here, selenium attenuated cell viability and increased cell apoptosis, especially in MSC, when compared with control group (p |
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In current study, we examined the effects of three types of selenium, sodium selenite (SSE), methylseleninic acid (MSA) and methylselenocysteine (MSC) on EC cell line Eca109. Here, selenium attenuated cell viability and increased cell apoptosis, especially in MSC, when compared with control group (p<0.05). Meanwhile, MSC and MSA, but no SSE, arrested cell cycle in G0/G1 phase (p<0.05). Mechanistically, FAL1 and PTEN were found to participate in regulating cell cycle and cell apoptosis process by decreasing cyclinD1, CDK2, and promoting caspase-3, caspase-8. In addition, we found that cyclinD1, CDK2 were significantly downregulated by MSA and MSC, while caspase-3, caspase-8 were dramatically upregulated by SSE (p<0.05). Based on these results, we concluded that MSC and MSA inhibit the viability of Eca109 mainly through reducing cell proliferation, while SSE by promoting apoptosis.</description><identifier>ISSN: 0301-4800</identifier><identifier>EISSN: 1881-7742</identifier><identifier>DOI: 10.3177/jnsv.66.456</identifier><language>eng</language><publisher>Center for Academic Publications Japan</publisher><subject>apoptosis ; cell proliferation ; methylseleninic acid ; methylselenocysteine ; sodium selenite</subject><ispartof>Journal of Nutritional Science and Vitaminology, 2020/10/31, Vol.66(5), pp.456-461</ispartof><rights>2020 by the Center for Academic Publications Japan</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c532t-c2994482e9a371e086c5bc9842abdfc5e86886b71df69120f7725f221b99dfb13</citedby><cites>FETCH-LOGICAL-c532t-c2994482e9a371e086c5bc9842abdfc5e86886b71df69120f7725f221b99dfb13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,1877,27901,27902</link.rule.ids></links><search><creatorcontrib>LIU, Tao</creatorcontrib><creatorcontrib>SUN, Yu</creatorcontrib><creatorcontrib>YANG, Shengzhuang</creatorcontrib><creatorcontrib>LIANG, Xiangsen</creatorcontrib><title>Inhibitory Effect of Selenium on Esophagus Cancer Cells and the Related Mechanism</title><title>Journal of Nutritional Science and Vitaminology</title><addtitle>J Nutr Sci Vitaminol</addtitle><description>Selenium has been associated with many malignant tumors including esophagus cancer (EC). In current study, we examined the effects of three types of selenium, sodium selenite (SSE), methylseleninic acid (MSA) and methylselenocysteine (MSC) on EC cell line Eca109. Here, selenium attenuated cell viability and increased cell apoptosis, especially in MSC, when compared with control group (p<0.05). Meanwhile, MSC and MSA, but no SSE, arrested cell cycle in G0/G1 phase (p<0.05). Mechanistically, FAL1 and PTEN were found to participate in regulating cell cycle and cell apoptosis process by decreasing cyclinD1, CDK2, and promoting caspase-3, caspase-8. In addition, we found that cyclinD1, CDK2 were significantly downregulated by MSA and MSC, while caspase-3, caspase-8 were dramatically upregulated by SSE (p<0.05). Based on these results, we concluded that MSC and MSA inhibit the viability of Eca109 mainly through reducing cell proliferation, while SSE by promoting apoptosis.</description><subject>apoptosis</subject><subject>cell proliferation</subject><subject>methylseleninic acid</subject><subject>methylselenocysteine</subject><subject>sodium selenite</subject><issn>0301-4800</issn><issn>1881-7742</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><recordid>eNo9kF1LwzAUhoMoOKdX_oHcS2eSpkl6I0iZOpiIX9chTU_Wji4dSSbs39uxsatz8T7n8J4HoXtKZjmV8nHt499MiBkvxAWaUKVoJiVnl2hCckIzrgi5RjcxrgnhpeJqgj4Xvu3qLg1hj-fOgU14cPgbevDdboMHj-dx2LZmtYu4Mt5CwBX0fcTGNzi1gL-gNwka_A62Nb6Lm1t05Uwf4e40p-j3Zf5TvWXLj9dF9bzMbJGzlFlWlpwrBqXJJQWihC1qO5Zipm6cLUAJpUQtaeNESRlxUrLCMUbrsmxcTfMpejjetWGIMYDT29BtTNhrSvTBhj7Y0ELo0cZIPx3pdUxmBWfWhNTZHs5scVo4B-NXQYPP_wG3J2oe</recordid><startdate>20201031</startdate><enddate>20201031</enddate><creator>LIU, Tao</creator><creator>SUN, Yu</creator><creator>YANG, Shengzhuang</creator><creator>LIANG, Xiangsen</creator><general>Center for Academic Publications Japan</general><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>20201031</creationdate><title>Inhibitory Effect of Selenium on Esophagus Cancer Cells and the Related Mechanism</title><author>LIU, Tao ; SUN, Yu ; YANG, Shengzhuang ; LIANG, Xiangsen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c532t-c2994482e9a371e086c5bc9842abdfc5e86886b71df69120f7725f221b99dfb13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>apoptosis</topic><topic>cell proliferation</topic><topic>methylseleninic acid</topic><topic>methylselenocysteine</topic><topic>sodium selenite</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>LIU, Tao</creatorcontrib><creatorcontrib>SUN, Yu</creatorcontrib><creatorcontrib>YANG, Shengzhuang</creatorcontrib><creatorcontrib>LIANG, Xiangsen</creatorcontrib><collection>CrossRef</collection><jtitle>Journal of Nutritional Science and Vitaminology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>LIU, Tao</au><au>SUN, Yu</au><au>YANG, Shengzhuang</au><au>LIANG, Xiangsen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibitory Effect of Selenium on Esophagus Cancer Cells and the Related Mechanism</atitle><jtitle>Journal of Nutritional Science and Vitaminology</jtitle><addtitle>J Nutr Sci Vitaminol</addtitle><date>2020-10-31</date><risdate>2020</risdate><volume>66</volume><issue>5</issue><spage>456</spage><epage>461</epage><pages>456-461</pages><issn>0301-4800</issn><eissn>1881-7742</eissn><abstract>Selenium has been associated with many malignant tumors including esophagus cancer (EC). In current study, we examined the effects of three types of selenium, sodium selenite (SSE), methylseleninic acid (MSA) and methylselenocysteine (MSC) on EC cell line Eca109. Here, selenium attenuated cell viability and increased cell apoptosis, especially in MSC, when compared with control group (p<0.05). Meanwhile, MSC and MSA, but no SSE, arrested cell cycle in G0/G1 phase (p<0.05). Mechanistically, FAL1 and PTEN were found to participate in regulating cell cycle and cell apoptosis process by decreasing cyclinD1, CDK2, and promoting caspase-3, caspase-8. In addition, we found that cyclinD1, CDK2 were significantly downregulated by MSA and MSC, while caspase-3, caspase-8 were dramatically upregulated by SSE (p<0.05). Based on these results, we concluded that MSC and MSA inhibit the viability of Eca109 mainly through reducing cell proliferation, while SSE by promoting apoptosis.</abstract><pub>Center for Academic Publications Japan</pub><doi>10.3177/jnsv.66.456</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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subjects | apoptosis cell proliferation methylseleninic acid methylselenocysteine sodium selenite |
title | Inhibitory Effect of Selenium on Esophagus Cancer Cells and the Related Mechanism |
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