Overexpression of GOLPH3 Promotes Proliferation and Tumorigenicity in Breast Cancer via Suppression of the FOXO1 Transcription Factor
Golgi phosphoprotein 3 (GOLPH3) has been reported to be involved in various biologic processes. The clinical significance and biologic role of GOLPH3 in breast cancer, however, remains unknown. Expression of GOLPH3 in normal breast cells, breast cancer cells, and 6-paired breast cancer and adjacent...
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| Veröffentlicht in: | Clinical cancer research 2012-08, Vol.18 (15), p.4059-4069 |
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| creator | Zeng, Zhaolei Lin, Huanxin Zhao, Xiaohui Liu, Guanglin Wang, Xi Xu, Ruihua Chen, Kun Li, Jun Song, Libing |
| description | Golgi phosphoprotein 3 (GOLPH3) has been reported to be involved in various biologic processes. The clinical significance and biologic role of GOLPH3 in breast cancer, however, remains unknown.
Expression of GOLPH3 in normal breast cells, breast cancer cells, and 6-paired breast cancer and adjacent noncancerous tissues were quantified using real-time PCR and Western blotting. GOLPH3 protein expression was analyzed in 258 archived, paraffin-embedded breast cancer samples using immunohistochemistry. The role of GOLPH3 in breast cancer cell proliferation and tumorigenicity was explored in vitro and in vivo. Western blotting and luciferase reporter analyses were used to investigate the effect of GOLPH3 overexpression and silencing on the expression of cell-cycle regulators and FOXO1 transcriptional activity.
GOLPH3 was significantly upregulated in breast cancer cells and tissues compared with normal cells and tissues. Immunohistochemical analysis revealed high expression of GOLPH3 in 133 of 258 (51.6%) breast cancer specimens. Statistical analysis showed a significant correlation of GOLPH3 expression with advanced clinical stage and poorer survival. Overexpression and ablation of GOLPH3 promoted and inhibited, respectively, the proliferation and tumorigenicity of breast cancer cells in vitro and in vivo. GOLPH3 overexpression enhanced AKT activity and decreased FOXO1 transcriptional activity, downregulated cyclin-dependent kinase (CDK) inhibitor p21(Cip1), p27(Kip1), and p57(Kip2), and upregulated the CDK regulator cyclin D1.
Our results suggest that high GOLPH3 expression is associated with poor overall survival in patients with breast cancer and that GOLPH3 overexpression increases the proliferation and tumorigenicity of human breast cancer cells. |
| doi_str_mv | 10.1158/1078-0432.ccr-11-3156 |
| format | Article |
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Expression of GOLPH3 in normal breast cells, breast cancer cells, and 6-paired breast cancer and adjacent noncancerous tissues were quantified using real-time PCR and Western blotting. GOLPH3 protein expression was analyzed in 258 archived, paraffin-embedded breast cancer samples using immunohistochemistry. The role of GOLPH3 in breast cancer cell proliferation and tumorigenicity was explored in vitro and in vivo. Western blotting and luciferase reporter analyses were used to investigate the effect of GOLPH3 overexpression and silencing on the expression of cell-cycle regulators and FOXO1 transcriptional activity.
GOLPH3 was significantly upregulated in breast cancer cells and tissues compared with normal cells and tissues. Immunohistochemical analysis revealed high expression of GOLPH3 in 133 of 258 (51.6%) breast cancer specimens. Statistical analysis showed a significant correlation of GOLPH3 expression with advanced clinical stage and poorer survival. Overexpression and ablation of GOLPH3 promoted and inhibited, respectively, the proliferation and tumorigenicity of breast cancer cells in vitro and in vivo. GOLPH3 overexpression enhanced AKT activity and decreased FOXO1 transcriptional activity, downregulated cyclin-dependent kinase (CDK) inhibitor p21(Cip1), p27(Kip1), and p57(Kip2), and upregulated the CDK regulator cyclin D1.
Our results suggest that high GOLPH3 expression is associated with poor overall survival in patients with breast cancer and that GOLPH3 overexpression increases the proliferation and tumorigenicity of human breast cancer cells.</description><identifier>ISSN: 1078-0432</identifier><identifier>EISSN: 1557-3265</identifier><identifier>DOI: 10.1158/1078-0432.ccr-11-3156</identifier><identifier>PMID: 22675169</identifier><identifier>CODEN: CCREF4</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Animals ; Antineoplastic agents ; Biological and medical sciences ; Blotting, Western ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Cell Cycle - genetics ; Cell Line ; Cell Line, Tumor ; Cell Proliferation ; Cell Transformation, Neoplastic - genetics ; Cell Transformation, Neoplastic - metabolism ; Cyclin-Dependent Kinase Inhibitor Proteins - genetics ; Cyclin-Dependent Kinase Inhibitor Proteins - metabolism ; Female ; Forkhead Box Protein O1 ; Forkhead Transcription Factors - genetics ; Forkhead Transcription Factors - metabolism ; Gene Expression Regulation, Neoplastic ; Gynecology. Andrology. Obstetrics ; Humans ; Immunohistochemistry ; Kaplan-Meier Estimate ; Ki-67 Antigen - metabolism ; Mammary gland diseases ; Medical sciences ; Membrane Proteins - genetics ; Membrane Proteins - metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Middle Aged ; Pharmacology. Drug treatments ; Reverse Transcriptase Polymerase Chain Reaction ; RNA Interference ; Transplantation, Heterologous ; Tumors</subject><ispartof>Clinical cancer research, 2012-08, Vol.18 (15), p.4059-4069</ispartof><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c452t-373468c50f8dce944888c51a19739718cc623a9fd4209aaf38fb698f652c61263</citedby><cites>FETCH-LOGICAL-c452t-373468c50f8dce944888c51a19739718cc623a9fd4209aaf38fb698f652c61263</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3343,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26233897$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22675169$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zeng, Zhaolei</creatorcontrib><creatorcontrib>Lin, Huanxin</creatorcontrib><creatorcontrib>Zhao, Xiaohui</creatorcontrib><creatorcontrib>Liu, Guanglin</creatorcontrib><creatorcontrib>Wang, Xi</creatorcontrib><creatorcontrib>Xu, Ruihua</creatorcontrib><creatorcontrib>Chen, Kun</creatorcontrib><creatorcontrib>Li, Jun</creatorcontrib><creatorcontrib>Song, Libing</creatorcontrib><title>Overexpression of GOLPH3 Promotes Proliferation and Tumorigenicity in Breast Cancer via Suppression of the FOXO1 Transcription Factor</title><title>Clinical cancer research</title><addtitle>Clin Cancer Res</addtitle><description>Golgi phosphoprotein 3 (GOLPH3) has been reported to be involved in various biologic processes. The clinical significance and biologic role of GOLPH3 in breast cancer, however, remains unknown.
Expression of GOLPH3 in normal breast cells, breast cancer cells, and 6-paired breast cancer and adjacent noncancerous tissues were quantified using real-time PCR and Western blotting. GOLPH3 protein expression was analyzed in 258 archived, paraffin-embedded breast cancer samples using immunohistochemistry. The role of GOLPH3 in breast cancer cell proliferation and tumorigenicity was explored in vitro and in vivo. Western blotting and luciferase reporter analyses were used to investigate the effect of GOLPH3 overexpression and silencing on the expression of cell-cycle regulators and FOXO1 transcriptional activity.
GOLPH3 was significantly upregulated in breast cancer cells and tissues compared with normal cells and tissues. Immunohistochemical analysis revealed high expression of GOLPH3 in 133 of 258 (51.6%) breast cancer specimens. Statistical analysis showed a significant correlation of GOLPH3 expression with advanced clinical stage and poorer survival. Overexpression and ablation of GOLPH3 promoted and inhibited, respectively, the proliferation and tumorigenicity of breast cancer cells in vitro and in vivo. GOLPH3 overexpression enhanced AKT activity and decreased FOXO1 transcriptional activity, downregulated cyclin-dependent kinase (CDK) inhibitor p21(Cip1), p27(Kip1), and p57(Kip2), and upregulated the CDK regulator cyclin D1.
Our results suggest that high GOLPH3 expression is associated with poor overall survival in patients with breast cancer and that GOLPH3 overexpression increases the proliferation and tumorigenicity of human breast cancer cells.</description><subject>Animals</subject><subject>Antineoplastic agents</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Cell Cycle - genetics</subject><subject>Cell Line</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Cell Transformation, Neoplastic - genetics</subject><subject>Cell Transformation, Neoplastic - metabolism</subject><subject>Cyclin-Dependent Kinase Inhibitor Proteins - genetics</subject><subject>Cyclin-Dependent Kinase Inhibitor Proteins - metabolism</subject><subject>Female</subject><subject>Forkhead Box Protein O1</subject><subject>Forkhead Transcription Factors - genetics</subject><subject>Forkhead Transcription Factors - metabolism</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Kaplan-Meier Estimate</subject><subject>Ki-67 Antigen - metabolism</subject><subject>Mammary gland diseases</subject><subject>Medical sciences</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Middle Aged</subject><subject>Pharmacology. Drug treatments</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA Interference</subject><subject>Transplantation, Heterologous</subject><subject>Tumors</subject><issn>1078-0432</issn><issn>1557-3265</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkctO3TAQhi3UCijtI4C8qcQm4PEtzrKNOFDpSEFwKnUXGR8bXCVxaicIHqDvXaccSldz0Tf_aP5B6BjIGYBQ50BKVRDO6JkxsQAoGAi5hw5BiLJgVIp3OX9lDtCHlH4SAhwI30cHlMpSgKwO0e_m0Ub7NEabkg8DDg5fNuvrK4avY-jDZNOSdN7ZqKcF0MMWb-Y-RH9vB2_89Iz9gL9Gq9OEaz0YG_Gj1_h2Hv8XnR4sXjU_GsCbqIdkoh__yq20mUL8iN473SX7aReP0PfVxaa-KtbN5bf6y7owXNCpYCXjUhlBnNoaW3GuVK5AQ1WyqgRljKRMV27LKam0dky5O1kpJwU1EqhkR-j0RXeM4dds09T2PhnbdXqwYU4tEEZUyRVlGRUvqIkhpWhdO0bf6_icoXb5QLu42y7utnV9k1vt8oE8d7JbMd_1dvtv6tXyDHzeAToZ3blsh_HpjcsnMJUP-gOKEI90</recordid><startdate>20120801</startdate><enddate>20120801</enddate><creator>Zeng, Zhaolei</creator><creator>Lin, Huanxin</creator><creator>Zhao, Xiaohui</creator><creator>Liu, Guanglin</creator><creator>Wang, Xi</creator><creator>Xu, Ruihua</creator><creator>Chen, Kun</creator><creator>Li, Jun</creator><creator>Song, Libing</creator><general>American Association for Cancer Research</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></search><sort><creationdate>20120801</creationdate><title>Overexpression of GOLPH3 Promotes Proliferation and Tumorigenicity in Breast Cancer via Suppression of the FOXO1 Transcription Factor</title><author>Zeng, Zhaolei ; Lin, Huanxin ; Zhao, Xiaohui ; Liu, Guanglin ; Wang, Xi ; Xu, Ruihua ; Chen, Kun ; Li, Jun ; Song, Libing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c452t-373468c50f8dce944888c51a19739718cc623a9fd4209aaf38fb698f652c61263</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Animals</topic><topic>Antineoplastic agents</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Cell Cycle - genetics</topic><topic>Cell Line</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Cell Transformation, Neoplastic - genetics</topic><topic>Cell Transformation, Neoplastic - metabolism</topic><topic>Cyclin-Dependent Kinase Inhibitor Proteins - genetics</topic><topic>Cyclin-Dependent Kinase Inhibitor Proteins - metabolism</topic><topic>Female</topic><topic>Forkhead Box Protein O1</topic><topic>Forkhead Transcription Factors - genetics</topic><topic>Forkhead Transcription Factors - metabolism</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Kaplan-Meier Estimate</topic><topic>Ki-67 Antigen - metabolism</topic><topic>Mammary gland diseases</topic><topic>Medical sciences</topic><topic>Membrane Proteins - genetics</topic><topic>Membrane Proteins - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>Middle Aged</topic><topic>Pharmacology. Drug treatments</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA Interference</topic><topic>Transplantation, Heterologous</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zeng, Zhaolei</creatorcontrib><creatorcontrib>Lin, Huanxin</creatorcontrib><creatorcontrib>Zhao, Xiaohui</creatorcontrib><creatorcontrib>Liu, Guanglin</creatorcontrib><creatorcontrib>Wang, Xi</creatorcontrib><creatorcontrib>Xu, Ruihua</creatorcontrib><creatorcontrib>Chen, Kun</creatorcontrib><creatorcontrib>Li, Jun</creatorcontrib><creatorcontrib>Song, Libing</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><jtitle>Clinical cancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zeng, Zhaolei</au><au>Lin, Huanxin</au><au>Zhao, Xiaohui</au><au>Liu, Guanglin</au><au>Wang, Xi</au><au>Xu, Ruihua</au><au>Chen, Kun</au><au>Li, Jun</au><au>Song, Libing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Overexpression of GOLPH3 Promotes Proliferation and Tumorigenicity in Breast Cancer via Suppression of the FOXO1 Transcription Factor</atitle><jtitle>Clinical cancer research</jtitle><addtitle>Clin Cancer Res</addtitle><date>2012-08-01</date><risdate>2012</risdate><volume>18</volume><issue>15</issue><spage>4059</spage><epage>4069</epage><pages>4059-4069</pages><issn>1078-0432</issn><eissn>1557-3265</eissn><coden>CCREF4</coden><abstract>Golgi phosphoprotein 3 (GOLPH3) has been reported to be involved in various biologic processes. The clinical significance and biologic role of GOLPH3 in breast cancer, however, remains unknown.
Expression of GOLPH3 in normal breast cells, breast cancer cells, and 6-paired breast cancer and adjacent noncancerous tissues were quantified using real-time PCR and Western blotting. GOLPH3 protein expression was analyzed in 258 archived, paraffin-embedded breast cancer samples using immunohistochemistry. The role of GOLPH3 in breast cancer cell proliferation and tumorigenicity was explored in vitro and in vivo. Western blotting and luciferase reporter analyses were used to investigate the effect of GOLPH3 overexpression and silencing on the expression of cell-cycle regulators and FOXO1 transcriptional activity.
GOLPH3 was significantly upregulated in breast cancer cells and tissues compared with normal cells and tissues. Immunohistochemical analysis revealed high expression of GOLPH3 in 133 of 258 (51.6%) breast cancer specimens. Statistical analysis showed a significant correlation of GOLPH3 expression with advanced clinical stage and poorer survival. Overexpression and ablation of GOLPH3 promoted and inhibited, respectively, the proliferation and tumorigenicity of breast cancer cells in vitro and in vivo. GOLPH3 overexpression enhanced AKT activity and decreased FOXO1 transcriptional activity, downregulated cyclin-dependent kinase (CDK) inhibitor p21(Cip1), p27(Kip1), and p57(Kip2), and upregulated the CDK regulator cyclin D1.
Our results suggest that high GOLPH3 expression is associated with poor overall survival in patients with breast cancer and that GOLPH3 overexpression increases the proliferation and tumorigenicity of human breast cancer cells.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>22675169</pmid><doi>10.1158/1078-0432.ccr-11-3156</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antineoplastic agents Biological and medical sciences Blotting, Western Breast Neoplasms - genetics Breast Neoplasms - metabolism Breast Neoplasms - pathology Cell Cycle - genetics Cell Line Cell Line, Tumor Cell Proliferation Cell Transformation, Neoplastic - genetics Cell Transformation, Neoplastic - metabolism Cyclin-Dependent Kinase Inhibitor Proteins - genetics Cyclin-Dependent Kinase Inhibitor Proteins - metabolism Female Forkhead Box Protein O1 Forkhead Transcription Factors - genetics Forkhead Transcription Factors - metabolism Gene Expression Regulation, Neoplastic Gynecology. Andrology. Obstetrics Humans Immunohistochemistry Kaplan-Meier Estimate Ki-67 Antigen - metabolism Mammary gland diseases Medical sciences Membrane Proteins - genetics Membrane Proteins - metabolism Mice Mice, Inbred BALB C Mice, Nude Middle Aged Pharmacology. Drug treatments Reverse Transcriptase Polymerase Chain Reaction RNA Interference Transplantation, Heterologous Tumors |
| title | Overexpression of GOLPH3 Promotes Proliferation and Tumorigenicity in Breast Cancer via Suppression of the FOXO1 Transcription Factor |
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