Cell cycle‐related kinase supports ovarian carcinoma cell proliferation via regulation of cyclin D1 and is a predictor of outcome in patients with ovarian carcinoma
Our previous study has suggested that the cell cycle‐related kinase (CCRK) is a putative candidate oncogene in glioblastoma tumorigenesis. The potential oncogenic role of CCRK and its clinical/prognostic significance, however, in ovarian carcinoma are unclear. In this study, CCRK expression was exam...
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| creator | Wu, Guo‐Qing Xie, Dan Yang, Guo‐Feng Liao, Yi‐Ji Mai, Shi‐Juan Deng, Hai‐Xia Sze, Johnny Guan, Xin‐Yuan Zeng, Yi‐Xin Lin, Marie C. Kung, Hsiang‐Fu |
| description | Our previous study has suggested that the cell cycle‐related kinase (CCRK) is a putative candidate oncogene in glioblastoma tumorigenesis. The potential oncogenic role of CCRK and its clinical/prognostic significance, however, in ovarian carcinoma are unclear. In this study, CCRK expression was examined by immunohistochemistry in a series of ovarian carcinoma tissues. Overexpression of CCRK was detected in 53% of the ovarian carcinomas, and it was positively correlated with an ascending histological grade and/or advanced clinical stage of the disease (p < 0.05). In addition, overexpression of CCRK in ovarian carcinoma was determined to be a strong and an independent predictor of short overall survival (p < 0.05). In ovarian carcinoma cells, CCRK knockdown by RNAi led to a G1 phase cell cycle arrest, while CCRK overexpression by stable transfection of CCRK‐containing plasmid pcDNA‐CCRK promoted cell proliferation in vitro and tumor growth in vivo. In addition, CCRK knockdown was found to reduce cyclin D1 expression. Consistently, CCRK overexpression increased cyclin D1 expression, and furthermore, a significant correlation between expression of CCRK and cyclin D1 in ovarian carcinomas was observed (p < 0.001). These findings suggest a potential important role of CCRK in the control of cell proliferation via regulation of cyclin D1 expression, and the overexpression of CCRK, as detected by immunohistochemistry, is an independent molecular marker for shortened survival time of patients with ovarian carcinoma. © 2009 UICC |
| doi_str_mv | 10.1002/ijc.24630 |
| format | Article |
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The potential oncogenic role of CCRK and its clinical/prognostic significance, however, in ovarian carcinoma are unclear. In this study, CCRK expression was examined by immunohistochemistry in a series of ovarian carcinoma tissues. Overexpression of CCRK was detected in 53% of the ovarian carcinomas, and it was positively correlated with an ascending histological grade and/or advanced clinical stage of the disease (p < 0.05). In addition, overexpression of CCRK in ovarian carcinoma was determined to be a strong and an independent predictor of short overall survival (p < 0.05). In ovarian carcinoma cells, CCRK knockdown by RNAi led to a G1 phase cell cycle arrest, while CCRK overexpression by stable transfection of CCRK‐containing plasmid pcDNA‐CCRK promoted cell proliferation in vitro and tumor growth in vivo. In addition, CCRK knockdown was found to reduce cyclin D1 expression. Consistently, CCRK overexpression increased cyclin D1 expression, and furthermore, a significant correlation between expression of CCRK and cyclin D1 in ovarian carcinomas was observed (p < 0.001). These findings suggest a potential important role of CCRK in the control of cell proliferation via regulation of cyclin D1 expression, and the overexpression of CCRK, as detected by immunohistochemistry, is an independent molecular marker for shortened survival time of patients with ovarian carcinoma. © 2009 UICC</description><identifier>ISSN: 0020-7136</identifier><identifier>EISSN: 1097-0215</identifier><identifier>DOI: 10.1002/ijc.24630</identifier><identifier>PMID: 19672860</identifier><identifier>CODEN: IJCNAW</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Adult ; Aged ; Animals ; Apoptosis ; Biological and medical sciences ; Blotting, Western ; Case-Control Studies ; cell cycle ; cell cycle‐related kinase ; Cell Proliferation ; Cohort Studies ; cyclin D1 ; Cyclin D1 - metabolism ; Cyclin-Dependent Kinases - antagonists & inhibitors ; Cyclin-Dependent Kinases - genetics ; Cyclin-Dependent Kinases - metabolism ; Cystadenocarcinoma, Serous - genetics ; Cystadenocarcinoma, Serous - metabolism ; Cystadenocarcinoma, Serous - secondary ; Female ; Female genital diseases ; Gene Expression Regulation, Neoplastic ; Gynecology. Andrology. Obstetrics ; Humans ; Immunoenzyme Techniques ; Medical sciences ; Mice ; Mice, Inbred BALB C ; Middle Aged ; ovarian cancer ; Ovarian Neoplasms - genetics ; Ovarian Neoplasms - metabolism ; Ovarian Neoplasms - pathology ; Ovary - metabolism ; Ovary - pathology ; Phosphorylation ; Prognosis ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; RNA, Small Interfering - pharmacology ; Survival Rate ; Tissue Array Analysis ; Tumor Cells, Cultured ; Tumors</subject><ispartof>International journal of cancer, 2009-12, Vol.125 (11), p.2631-2642</ispartof><rights>Copyright © 2009 UICC</rights><rights>2009 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3850-4a2198f7c298a325f5ebc827274939d30af5067d0ada03b3db0471b6d910dd813</citedby><cites>FETCH-LOGICAL-c3850-4a2198f7c298a325f5ebc827274939d30af5067d0ada03b3db0471b6d910dd813</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fijc.24630$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fijc.24630$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22037232$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19672860$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Guo‐Qing</creatorcontrib><creatorcontrib>Xie, Dan</creatorcontrib><creatorcontrib>Yang, Guo‐Feng</creatorcontrib><creatorcontrib>Liao, Yi‐Ji</creatorcontrib><creatorcontrib>Mai, Shi‐Juan</creatorcontrib><creatorcontrib>Deng, Hai‐Xia</creatorcontrib><creatorcontrib>Sze, Johnny</creatorcontrib><creatorcontrib>Guan, Xin‐Yuan</creatorcontrib><creatorcontrib>Zeng, Yi‐Xin</creatorcontrib><creatorcontrib>Lin, Marie C.</creatorcontrib><creatorcontrib>Kung, Hsiang‐Fu</creatorcontrib><title>Cell cycle‐related kinase supports ovarian carcinoma cell proliferation via regulation of cyclin D1 and is a predictor of outcome in patients with ovarian carcinoma</title><title>International journal of cancer</title><addtitle>Int J Cancer</addtitle><description>Our previous study has suggested that the cell cycle‐related kinase (CCRK) is a putative candidate oncogene in glioblastoma tumorigenesis. The potential oncogenic role of CCRK and its clinical/prognostic significance, however, in ovarian carcinoma are unclear. In this study, CCRK expression was examined by immunohistochemistry in a series of ovarian carcinoma tissues. Overexpression of CCRK was detected in 53% of the ovarian carcinomas, and it was positively correlated with an ascending histological grade and/or advanced clinical stage of the disease (p < 0.05). In addition, overexpression of CCRK in ovarian carcinoma was determined to be a strong and an independent predictor of short overall survival (p < 0.05). In ovarian carcinoma cells, CCRK knockdown by RNAi led to a G1 phase cell cycle arrest, while CCRK overexpression by stable transfection of CCRK‐containing plasmid pcDNA‐CCRK promoted cell proliferation in vitro and tumor growth in vivo. In addition, CCRK knockdown was found to reduce cyclin D1 expression. Consistently, CCRK overexpression increased cyclin D1 expression, and furthermore, a significant correlation between expression of CCRK and cyclin D1 in ovarian carcinomas was observed (p < 0.001). These findings suggest a potential important role of CCRK in the control of cell proliferation via regulation of cyclin D1 expression, and the overexpression of CCRK, as detected by immunohistochemistry, is an independent molecular marker for shortened survival time of patients with ovarian carcinoma. © 2009 UICC</description><subject>Adult</subject><subject>Aged</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Case-Control Studies</subject><subject>cell cycle</subject><subject>cell cycle‐related kinase</subject><subject>Cell Proliferation</subject><subject>Cohort Studies</subject><subject>cyclin D1</subject><subject>Cyclin D1 - metabolism</subject><subject>Cyclin-Dependent Kinases - antagonists & inhibitors</subject><subject>Cyclin-Dependent Kinases - genetics</subject><subject>Cyclin-Dependent Kinases - metabolism</subject><subject>Cystadenocarcinoma, Serous - genetics</subject><subject>Cystadenocarcinoma, Serous - metabolism</subject><subject>Cystadenocarcinoma, Serous - secondary</subject><subject>Female</subject><subject>Female genital diseases</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Immunoenzyme Techniques</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Middle Aged</subject><subject>ovarian cancer</subject><subject>Ovarian Neoplasms - genetics</subject><subject>Ovarian Neoplasms - metabolism</subject><subject>Ovarian Neoplasms - pathology</subject><subject>Ovary - metabolism</subject><subject>Ovary - pathology</subject><subject>Phosphorylation</subject><subject>Prognosis</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>RNA, Small Interfering - pharmacology</subject><subject>Survival Rate</subject><subject>Tissue Array Analysis</subject><subject>Tumor Cells, Cultured</subject><subject>Tumors</subject><issn>0020-7136</issn><issn>1097-0215</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc1u1TAQhS0EoreFBS-AvIGKRdqxndjJsrr8FVViA-toYjvg4sTBTlrdHY_AU_BgPAm-zRUsEKwsa75zzowOIU8YnDEAfu6u9RkvpYB7ZMOgUQVwVt0nmzyDQjEhj8hxStcAjFVQPiRHrJGK1xI25MfWek_1Tnv789v3aD3O1tAvbsRkaVqmKcQ50XCD0eFINUbtxjAg1XvZFIN3vY04uzDSG4c02k-LX7-hv7N1I33JKI6GukQxS6xxeg5xPw_LrMNgaWamLLJjjrp18-e_8x6RBz36ZB8f3hPy8fWrD9u3xdX7N5fbi6tCi7qCokTOmrpXmjc1Cl71le10zRVXZSMaIwD7CqQygAZBdMJ0UCrWSdMwMKZm4oScrr75tK-LTXM7uLS_FUcbltSqUgITJYdMPv8vKZVUSpYqgy9WUMeQUrR9O0U3YNy1DNp9fW2ur72rL7NPD6ZLN1jzhzz0lYFnBwCTRt9HHLVLvzmeF1Nc8Mydr9yt83b378T28t12jf4FGMC0SA</recordid><startdate>20091201</startdate><enddate>20091201</enddate><creator>Wu, Guo‐Qing</creator><creator>Xie, Dan</creator><creator>Yang, Guo‐Feng</creator><creator>Liao, Yi‐Ji</creator><creator>Mai, Shi‐Juan</creator><creator>Deng, Hai‐Xia</creator><creator>Sze, Johnny</creator><creator>Guan, Xin‐Yuan</creator><creator>Zeng, Yi‐Xin</creator><creator>Lin, Marie C.</creator><creator>Kung, Hsiang‐Fu</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley-Blackwell</general><scope>IQODW</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>7X8</scope><scope>7TO</scope><scope>H94</scope></search><sort><creationdate>20091201</creationdate><title>Cell cycle‐related kinase supports ovarian carcinoma cell proliferation via regulation of cyclin D1 and is a predictor of outcome in patients with ovarian carcinoma</title><author>Wu, Guo‐Qing ; Xie, Dan ; Yang, Guo‐Feng ; Liao, Yi‐Ji ; Mai, Shi‐Juan ; Deng, Hai‐Xia ; Sze, Johnny ; Guan, Xin‐Yuan ; Zeng, Yi‐Xin ; Lin, Marie C. ; Kung, Hsiang‐Fu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3850-4a2198f7c298a325f5ebc827274939d30af5067d0ada03b3db0471b6d910dd813</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Case-Control Studies</topic><topic>cell cycle</topic><topic>cell cycle‐related kinase</topic><topic>Cell Proliferation</topic><topic>Cohort Studies</topic><topic>cyclin D1</topic><topic>Cyclin D1 - metabolism</topic><topic>Cyclin-Dependent Kinases - antagonists & inhibitors</topic><topic>Cyclin-Dependent Kinases - genetics</topic><topic>Cyclin-Dependent Kinases - metabolism</topic><topic>Cystadenocarcinoma, Serous - genetics</topic><topic>Cystadenocarcinoma, Serous - metabolism</topic><topic>Cystadenocarcinoma, Serous - secondary</topic><topic>Female</topic><topic>Female genital diseases</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Immunoenzyme Techniques</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Middle Aged</topic><topic>ovarian cancer</topic><topic>Ovarian Neoplasms - genetics</topic><topic>Ovarian Neoplasms - metabolism</topic><topic>Ovarian Neoplasms - pathology</topic><topic>Ovary - metabolism</topic><topic>Ovary - pathology</topic><topic>Phosphorylation</topic><topic>Prognosis</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>RNA, Small Interfering - pharmacology</topic><topic>Survival Rate</topic><topic>Tissue Array Analysis</topic><topic>Tumor Cells, Cultured</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Guo‐Qing</creatorcontrib><creatorcontrib>Xie, Dan</creatorcontrib><creatorcontrib>Yang, Guo‐Feng</creatorcontrib><creatorcontrib>Liao, Yi‐Ji</creatorcontrib><creatorcontrib>Mai, Shi‐Juan</creatorcontrib><creatorcontrib>Deng, Hai‐Xia</creatorcontrib><creatorcontrib>Sze, Johnny</creatorcontrib><creatorcontrib>Guan, Xin‐Yuan</creatorcontrib><creatorcontrib>Zeng, Yi‐Xin</creatorcontrib><creatorcontrib>Lin, Marie C.</creatorcontrib><creatorcontrib>Kung, Hsiang‐Fu</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>International journal of cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Guo‐Qing</au><au>Xie, Dan</au><au>Yang, Guo‐Feng</au><au>Liao, Yi‐Ji</au><au>Mai, Shi‐Juan</au><au>Deng, Hai‐Xia</au><au>Sze, Johnny</au><au>Guan, Xin‐Yuan</au><au>Zeng, Yi‐Xin</au><au>Lin, Marie C.</au><au>Kung, Hsiang‐Fu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cell cycle‐related kinase supports ovarian carcinoma cell proliferation via regulation of cyclin D1 and is a predictor of outcome in patients with ovarian carcinoma</atitle><jtitle>International journal of cancer</jtitle><addtitle>Int J Cancer</addtitle><date>2009-12-01</date><risdate>2009</risdate><volume>125</volume><issue>11</issue><spage>2631</spage><epage>2642</epage><pages>2631-2642</pages><issn>0020-7136</issn><eissn>1097-0215</eissn><coden>IJCNAW</coden><abstract>Our previous study has suggested that the cell cycle‐related kinase (CCRK) is a putative candidate oncogene in glioblastoma tumorigenesis. The potential oncogenic role of CCRK and its clinical/prognostic significance, however, in ovarian carcinoma are unclear. In this study, CCRK expression was examined by immunohistochemistry in a series of ovarian carcinoma tissues. Overexpression of CCRK was detected in 53% of the ovarian carcinomas, and it was positively correlated with an ascending histological grade and/or advanced clinical stage of the disease (p < 0.05). In addition, overexpression of CCRK in ovarian carcinoma was determined to be a strong and an independent predictor of short overall survival (p < 0.05). In ovarian carcinoma cells, CCRK knockdown by RNAi led to a G1 phase cell cycle arrest, while CCRK overexpression by stable transfection of CCRK‐containing plasmid pcDNA‐CCRK promoted cell proliferation in vitro and tumor growth in vivo. In addition, CCRK knockdown was found to reduce cyclin D1 expression. Consistently, CCRK overexpression increased cyclin D1 expression, and furthermore, a significant correlation between expression of CCRK and cyclin D1 in ovarian carcinomas was observed (p < 0.001). These findings suggest a potential important role of CCRK in the control of cell proliferation via regulation of cyclin D1 expression, and the overexpression of CCRK, as detected by immunohistochemistry, is an independent molecular marker for shortened survival time of patients with ovarian carcinoma. © 2009 UICC</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>19672860</pmid><doi>10.1002/ijc.24630</doi><tpages>12</tpages></addata></record> |
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| subjects | Adult Aged Animals Apoptosis Biological and medical sciences Blotting, Western Case-Control Studies cell cycle cell cycle‐related kinase Cell Proliferation Cohort Studies cyclin D1 Cyclin D1 - metabolism Cyclin-Dependent Kinases - antagonists & inhibitors Cyclin-Dependent Kinases - genetics Cyclin-Dependent Kinases - metabolism Cystadenocarcinoma, Serous - genetics Cystadenocarcinoma, Serous - metabolism Cystadenocarcinoma, Serous - secondary Female Female genital diseases Gene Expression Regulation, Neoplastic Gynecology. Andrology. Obstetrics Humans Immunoenzyme Techniques Medical sciences Mice Mice, Inbred BALB C Middle Aged ovarian cancer Ovarian Neoplasms - genetics Ovarian Neoplasms - metabolism Ovarian Neoplasms - pathology Ovary - metabolism Ovary - pathology Phosphorylation Prognosis Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - genetics RNA, Messenger - metabolism RNA, Small Interfering - pharmacology Survival Rate Tissue Array Analysis Tumor Cells, Cultured Tumors |
| title | Cell cycle‐related kinase supports ovarian carcinoma cell proliferation via regulation of cyclin D1 and is a predictor of outcome in patients with ovarian carcinoma |
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