Overexpression of Aurora-A kinase promotes tumor cell proliferation and inhibits apoptosis in esophageal squamous cell carcinoma cell line
Attrora-A kinase, a serine/threonine protein kinase, is a potential oncogene. Amplification and overexpression of Aurora-A have been found in several types of human tumors, including esophageal squamous cell carcinoma （ESCC）. It has been demonstrated that cells overexpressing Attrora-A are more resi...
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| Veröffentlicht in: | Cell research 2006-04, Vol.16 (4), p.356-366 |
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| creator | Wang, Xiao Xia Liu, Rong Jin, Shun Qian Fan, Fei Yue Zhan, Qi Min |
| description | Attrora-A kinase, a serine/threonine protein kinase, is a potential oncogene. Amplification and overexpression of Aurora-A have been found in several types of human tumors, including esophageal squamous cell carcinoma （ESCC）. It has been demonstrated that cells overexpressing Attrora-A are more resistant to cisplatin-induced apoptosis. However, the molecular mechanisms mediating these effects remain largely unknown. In this report, we showed that overexpression of Attrora-A through stable transfection of pEGFP-Aurora-A in human ESCC KYSE150 cells significantly promoted cell proliferation and inhibited cisplatin- or UV irradiation-induced apoptosis. Cleavages of caspase-3 and poly （ADPribose） polymerase （PARP） in Attrora-A overexpressing cells were substantially reduced after cisplatin or UV treatment. Furthermore, we found that silencing of endogenous Aurora-A kinase with siRNA substantially enhanced sensitivity to cisplatin- or UV-induced apoptosis in human ESCC EC9706 cells. In parallel, overexpression of Aurora-A potently upregulated the expression of Bcl-2. Moreover, the knockdown of Bcl-2 by siRNA abrogated the Aurora-A＇s effect on inhibiting apoptosis. Taken together, these data provide evidence that Aurora-A overexpression promoting cell proliferation and inhibiting apoptosis, suggesting a novel mechanism that is closely related to malignant phenotype and anti-cancer drugs resistance of ESCC cells. |
| doi_str_mv | 10.1038/sj.cr.7310046 |
| format | Article |
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Amplification and overexpression of Aurora-A have been found in several types of human tumors, including esophageal squamous cell carcinoma （ESCC）. It has been demonstrated that cells overexpressing Attrora-A are more resistant to cisplatin-induced apoptosis. However, the molecular mechanisms mediating these effects remain largely unknown. In this report, we showed that overexpression of Attrora-A through stable transfection of pEGFP-Aurora-A in human ESCC KYSE150 cells significantly promoted cell proliferation and inhibited cisplatin- or UV irradiation-induced apoptosis. Cleavages of caspase-3 and poly （ADPribose） polymerase （PARP） in Attrora-A overexpressing cells were substantially reduced after cisplatin or UV treatment. Furthermore, we found that silencing of endogenous Aurora-A kinase with siRNA substantially enhanced sensitivity to cisplatin- or UV-induced apoptosis in human ESCC EC9706 cells. In parallel, overexpression of Aurora-A potently upregulated the expression of Bcl-2. Moreover, the knockdown of Bcl-2 by siRNA abrogated the Aurora-A＇s effect on inhibiting apoptosis. Taken together, these data provide evidence that Aurora-A overexpression promoting cell proliferation and inhibiting apoptosis, suggesting a novel mechanism that is closely related to malignant phenotype and anti-cancer drugs resistance of ESCC cells.</description><identifier>ISSN: 1001-0602</identifier><identifier>EISSN: 1748-7838</identifier><identifier>DOI: 10.1038/sj.cr.7310046</identifier><identifier>PMID: 16617331</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Apoptosis - drug effects ; Apoptosis - radiation effects ; Apoptosis Regulatory Proteins - genetics ; Aurora Kinases ; Biomedical and Life Sciences ; Caspase 3 ; Caspases - metabolism ; Cell Biology ; Cell Line, Tumor ; Cell Proliferation ; Cisplatin - antagonists & inhibitors ; Esophageal Neoplasms - genetics ; Humans ; Irradiation ; Life Sciences ; Neoplasms, Squamous Cell - genetics ; Neoplasms, Squamous Cell - metabolism ; Neoplastic Stem Cells ; original-article ; Poly(ADP-ribose) Polymerases - metabolism ; Protein-Serine-Threonine Kinases - genetics ; Protein-Serine-Threonine Kinases - metabolism ; Proto-Oncogene Proteins c-bcl-2 - genetics ; Radiation Tolerance - genetics ; RNA Interference - drug effects ; RNA Interference - radiation effects ; RNA, Small Interfering - drug effects ; RNA, Small Interfering - genetics ; RNA, Small Interfering - radiation effects ; Transfection ; Ultraviolet radiation ; Ultraviolet Rays ; 基因表达 ; 细胞增生 ; 肿瘤细胞 ; 食管细胞癌</subject><ispartof>Cell research, 2006-04, Vol.16 (4), p.356-366</ispartof><rights>Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences 2006</rights><rights>Copyright Nature Publishing Group Apr 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c446t-bed84f2b90ae254d4c78e173053ed19d65124d865066cf75039bb57d41949fe03</citedby><cites>FETCH-LOGICAL-c446t-bed84f2b90ae254d4c78e173053ed19d65124d865066cf75039bb57d41949fe03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://image.cqvip.com/vip1000/qk/85240X/85240X.jpg</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16617331$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Xiao Xia</creatorcontrib><creatorcontrib>Liu, Rong</creatorcontrib><creatorcontrib>Jin, Shun Qian</creatorcontrib><creatorcontrib>Fan, Fei Yue</creatorcontrib><creatorcontrib>Zhan, Qi Min</creatorcontrib><title>Overexpression of Aurora-A kinase promotes tumor cell proliferation and inhibits apoptosis in esophageal squamous cell carcinoma cell line</title><title>Cell research</title><addtitle>Cell Res</addtitle><addtitle>Cell Research</addtitle><description>Attrora-A kinase, a serine/threonine protein kinase, is a potential oncogene. Amplification and overexpression of Aurora-A have been found in several types of human tumors, including esophageal squamous cell carcinoma （ESCC）. It has been demonstrated that cells overexpressing Attrora-A are more resistant to cisplatin-induced apoptosis. However, the molecular mechanisms mediating these effects remain largely unknown. In this report, we showed that overexpression of Attrora-A through stable transfection of pEGFP-Aurora-A in human ESCC KYSE150 cells significantly promoted cell proliferation and inhibited cisplatin- or UV irradiation-induced apoptosis. Cleavages of caspase-3 and poly （ADPribose） polymerase （PARP） in Attrora-A overexpressing cells were substantially reduced after cisplatin or UV treatment. Furthermore, we found that silencing of endogenous Aurora-A kinase with siRNA substantially enhanced sensitivity to cisplatin- or UV-induced apoptosis in human ESCC EC9706 cells. In parallel, overexpression of Aurora-A potently upregulated the expression of Bcl-2. Moreover, the knockdown of Bcl-2 by siRNA abrogated the Aurora-A＇s effect on inhibiting apoptosis. Taken together, these data provide evidence that Aurora-A overexpression promoting cell proliferation and inhibiting apoptosis, suggesting a novel mechanism that is closely related to malignant phenotype and anti-cancer drugs resistance of ESCC cells.</description><subject>Apoptosis - drug effects</subject><subject>Apoptosis - radiation effects</subject><subject>Apoptosis Regulatory Proteins - genetics</subject><subject>Aurora Kinases</subject><subject>Biomedical and Life Sciences</subject><subject>Caspase 3</subject><subject>Caspases - metabolism</subject><subject>Cell Biology</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Cisplatin - antagonists & inhibitors</subject><subject>Esophageal Neoplasms - genetics</subject><subject>Humans</subject><subject>Irradiation</subject><subject>Life Sciences</subject><subject>Neoplasms, Squamous Cell - genetics</subject><subject>Neoplasms, Squamous Cell - metabolism</subject><subject>Neoplastic Stem Cells</subject><subject>original-article</subject><subject>Poly(ADP-ribose) Polymerases - metabolism</subject><subject>Protein-Serine-Threonine Kinases - genetics</subject><subject>Protein-Serine-Threonine Kinases - metabolism</subject><subject>Proto-Oncogene Proteins c-bcl-2 - genetics</subject><subject>Radiation Tolerance - genetics</subject><subject>RNA Interference - drug effects</subject><subject>RNA Interference - radiation effects</subject><subject>RNA, Small Interfering - drug effects</subject><subject>RNA, Small Interfering - genetics</subject><subject>RNA, Small Interfering - radiation effects</subject><subject>Transfection</subject><subject>Ultraviolet radiation</subject><subject>Ultraviolet Rays</subject><subject>基因表达</subject><subject>细胞增生</subject><subject>肿瘤细胞</subject><subject>食管细胞癌</subject><issn>1001-0602</issn><issn>1748-7838</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptkUFv1DAQhSMEoqVw5AiyqMQtix07tnNcVRSQKvUCZ8txJrveJnbWkyD4C_xqvMqKIsTJ9sw3z-9piuI1oxtGuf6Ah41LG8UZpUI-KS6ZErpUmuun-U4pK6mk1UXxAvFAaVWLmj0vLpiUTHHOLotf998hwY8pAaKPgcSebJcUky235MEHi0CmFMc4A5J5GWMiDobhVBt8D8nOpyEbOuLD3rd-RmKnOM0RPeYSAYzT3u7ADgSPix3jgquAs8n5EEe7Pgcf4GXxrLcDwqvzeVV8u_349eZzeXf_6cvN9q50Qsi5bKHToq_ahlrIeTrhlIachtYcOtZ0smaV6LSsqZSuVzXlTdvWqhOsEU0PlF8V71fdHOK4AM5m9HhyYQNkf0YqXfNKVRm8_gc8xCWF7M0wWimtGdUiU-VKuRQRE_RmSn606WeGzGlFBg_GJXNeUebfnlWXdoTukT7vJAObFcDcCjtIf3_7f8U360Cw85Lgj-Jj_93Z4T6G3TFrmta6h94PYCpWN0xVkv8G-yKzaA</recordid><startdate>20060401</startdate><enddate>20060401</enddate><creator>Wang, Xiao Xia</creator><creator>Liu, Rong</creator><creator>Jin, Shun Qian</creator><creator>Fan, Fei Yue</creator><creator>Zhan, Qi Min</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>2RA</scope><scope>92L</scope><scope>CQIGP</scope><scope>W91</scope><scope>~WA</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>7QO</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20060401</creationdate><title>Overexpression of Aurora-A kinase promotes tumor cell proliferation and inhibits apoptosis in esophageal squamous cell carcinoma cell line</title><author>Wang, Xiao Xia ; Liu, Rong ; Jin, Shun Qian ; Fan, Fei Yue ; Zhan, Qi Min</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c446t-bed84f2b90ae254d4c78e173053ed19d65124d865066cf75039bb57d41949fe03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Apoptosis - drug effects</topic><topic>Apoptosis - radiation effects</topic><topic>Apoptosis Regulatory Proteins - genetics</topic><topic>Aurora Kinases</topic><topic>Biomedical and Life Sciences</topic><topic>Caspase 3</topic><topic>Caspases - metabolism</topic><topic>Cell Biology</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Cisplatin - antagonists & inhibitors</topic><topic>Esophageal Neoplasms - genetics</topic><topic>Humans</topic><topic>Irradiation</topic><topic>Life Sciences</topic><topic>Neoplasms, Squamous Cell - genetics</topic><topic>Neoplasms, Squamous Cell - metabolism</topic><topic>Neoplastic Stem Cells</topic><topic>original-article</topic><topic>Poly(ADP-ribose) Polymerases - metabolism</topic><topic>Protein-Serine-Threonine Kinases - genetics</topic><topic>Protein-Serine-Threonine Kinases - metabolism</topic><topic>Proto-Oncogene Proteins c-bcl-2 - genetics</topic><topic>Radiation Tolerance - genetics</topic><topic>RNA Interference - drug effects</topic><topic>RNA Interference - 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Academic</collection><jtitle>Cell research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Xiao Xia</au><au>Liu, Rong</au><au>Jin, Shun Qian</au><au>Fan, Fei Yue</au><au>Zhan, Qi Min</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Overexpression of Aurora-A kinase promotes tumor cell proliferation and inhibits apoptosis in esophageal squamous cell carcinoma cell line</atitle><jtitle>Cell research</jtitle><stitle>Cell Res</stitle><addtitle>Cell Research</addtitle><date>2006-04-01</date><risdate>2006</risdate><volume>16</volume><issue>4</issue><spage>356</spage><epage>366</epage><pages>356-366</pages><issn>1001-0602</issn><eissn>1748-7838</eissn><abstract>Attrora-A kinase, a serine/threonine protein kinase, is a potential oncogene. Amplification and overexpression of Aurora-A have been found in several types of human tumors, including esophageal squamous cell carcinoma （ESCC）. It has been demonstrated that cells overexpressing Attrora-A are more resistant to cisplatin-induced apoptosis. However, the molecular mechanisms mediating these effects remain largely unknown. In this report, we showed that overexpression of Attrora-A through stable transfection of pEGFP-Aurora-A in human ESCC KYSE150 cells significantly promoted cell proliferation and inhibited cisplatin- or UV irradiation-induced apoptosis. Cleavages of caspase-3 and poly （ADPribose） polymerase （PARP） in Attrora-A overexpressing cells were substantially reduced after cisplatin or UV treatment. Furthermore, we found that silencing of endogenous Aurora-A kinase with siRNA substantially enhanced sensitivity to cisplatin- or UV-induced apoptosis in human ESCC EC9706 cells. In parallel, overexpression of Aurora-A potently upregulated the expression of Bcl-2. Moreover, the knockdown of Bcl-2 by siRNA abrogated the Aurora-A＇s effect on inhibiting apoptosis. Taken together, these data provide evidence that Aurora-A overexpression promoting cell proliferation and inhibiting apoptosis, suggesting a novel mechanism that is closely related to malignant phenotype and anti-cancer drugs resistance of ESCC cells.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>16617331</pmid><doi>10.1038/sj.cr.7310046</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Cell research, 2006-04, Vol.16 (4), p.356-366 |
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| subjects | Apoptosis - drug effects Apoptosis - radiation effects Apoptosis Regulatory Proteins - genetics Aurora Kinases Biomedical and Life Sciences Caspase 3 Caspases - metabolism Cell Biology Cell Line, Tumor Cell Proliferation Cisplatin - antagonists & inhibitors Esophageal Neoplasms - genetics Humans Irradiation Life Sciences Neoplasms, Squamous Cell - genetics Neoplasms, Squamous Cell - metabolism Neoplastic Stem Cells original-article Poly(ADP-ribose) Polymerases - metabolism Protein-Serine-Threonine Kinases - genetics Protein-Serine-Threonine Kinases - metabolism Proto-Oncogene Proteins c-bcl-2 - genetics Radiation Tolerance - genetics RNA Interference - drug effects RNA Interference - radiation effects RNA, Small Interfering - drug effects RNA, Small Interfering - genetics RNA, Small Interfering - radiation effects Transfection Ultraviolet radiation Ultraviolet Rays 基因表达 细胞增生 肿瘤细胞 食管细胞癌 |
| title | Overexpression of Aurora-A kinase promotes tumor cell proliferation and inhibits apoptosis in esophageal squamous cell carcinoma cell line |
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