Expression of caveolin-1 is correlated with lung adenocarcinoma proliferation, migration, and invasion
Both tumor suppressor and tumor promoter roles, which are dependent on the tumor type, have been described for caveolin-1 (CAV-1). Because CAV-1 can modulate cell signaling, we tested the hypothesis that it regulates lung adenocarcinoma cell proliferation and metastasis via modulation of epidermal g...
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| Veröffentlicht in: | Medical oncology (Northwood, London, England) London, England), 2015-07, Vol.32 (7), p.207-207, Article 207 |
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| creator | Luan, Tian-Yan Zhu, Tie-Nian Cui, Yu-Jie Zhang, Gang Song, Xue-Jing Gao, Dong-Mei Zhang, Yi-Mei Zhao, Qing-Lan Liu, Shuang Su, Tong-Yi Zhao, Rui-Jing |
| description | Both tumor suppressor and tumor promoter roles, which are dependent on the tumor type, have been described for caveolin-1 (CAV-1). Because CAV-1 can modulate cell signaling, we tested the hypothesis that it regulates lung adenocarcinoma cell proliferation and metastasis via modulation of epidermal growth factor receptor (EGFR) activity. The lung adenocarcinoma cell line, GLC-82, was transfected with pcDNA3.1CAV-1 plasmid, before cell proliferation, migration, and invasion were analyzed. In the in vivo xenograft model, the relationship between the CAV-1 expression and EGFR phosphorylation and signaling was assessed by western blot analysis. The relationship between the CAV-1 as well as Ki67 expression and the clinicopathological characteristics of 68 lung adenocarcinoma patients was also examined using immunohistochemistry. Overexpression of CAV-1 significantly increased GLC-82 proliferation (
p
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| doi_str_mv | 10.1007/s12032-015-0644-5 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1691015957</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3759892341</sourcerecordid><originalsourceid>FETCH-LOGICAL-c372t-8c413ee178359d4df8046179f34d2dba7bd19122526f6070eccdc8575aaf17c73</originalsourceid><addsrcrecordid>eNp1kUtr3TAQRkVoyfsHdFME3WQRtRrZsqxlCGkTCGTTQnZCV48bBVu6lew8_n1lblJCICsN6MyZYT6EvgD9DpSKHwUYbRihwAnt2pbwHbQPnEsCDdx-qnXDBaG8o3vooJR7ShlwJnfRHuuobKkQ-8hfPG2yKyWkiJPHRj-4NIRIAIeCTcrZDXpyFj-G6Q4Pc1xjbV1MRmcTYho13uTKe5f1VBWneAzr11JHi0N80Iv7CH32eiju-OU9RH9-Xvw-vyTXN7-uzs-uiWkEm0hvWmicA9E3XNrW-p62HQjpm9Yyu9JiZUECY5x1vqOCOmOs6bngWnsQRjSH6GTrrWv9nV2Z1BiKccOgo0tzUdBJqOeSfEG_vUPv05xj3W6hJAPWi7ZSsKVMTqVk59Umh1HnZwVULSGobQiqWtUSguK15-uLeV6Nzv7veL16BdgWKPUrrl1-M_pD6z-DiZIE</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1699212874</pqid></control><display><type>article</type><title>Expression of caveolin-1 is correlated with lung adenocarcinoma proliferation, migration, and invasion</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><creator>Luan, Tian-Yan ; Zhu, Tie-Nian ; Cui, Yu-Jie ; Zhang, Gang ; Song, Xue-Jing ; Gao, Dong-Mei ; Zhang, Yi-Mei ; Zhao, Qing-Lan ; Liu, Shuang ; Su, Tong-Yi ; Zhao, Rui-Jing</creator><creatorcontrib>Luan, Tian-Yan ; Zhu, Tie-Nian ; Cui, Yu-Jie ; Zhang, Gang ; Song, Xue-Jing ; Gao, Dong-Mei ; Zhang, Yi-Mei ; Zhao, Qing-Lan ; Liu, Shuang ; Su, Tong-Yi ; Zhao, Rui-Jing</creatorcontrib><description>Both tumor suppressor and tumor promoter roles, which are dependent on the tumor type, have been described for caveolin-1 (CAV-1). Because CAV-1 can modulate cell signaling, we tested the hypothesis that it regulates lung adenocarcinoma cell proliferation and metastasis via modulation of epidermal growth factor receptor (EGFR) activity. The lung adenocarcinoma cell line, GLC-82, was transfected with pcDNA3.1CAV-1 plasmid, before cell proliferation, migration, and invasion were analyzed. In the in vivo xenograft model, the relationship between the CAV-1 expression and EGFR phosphorylation and signaling was assessed by western blot analysis. The relationship between the CAV-1 as well as Ki67 expression and the clinicopathological characteristics of 68 lung adenocarcinoma patients was also examined using immunohistochemistry. Overexpression of CAV-1 significantly increased GLC-82 proliferation (
p
< 0.001), migration (
p
< 0.001), and invasion (
p
= 0.002) as well as EGFR and ERK phosphorylation (
p
< 0.05). The GLC-82/CAV-1 cell tumors were also significantly larger than those of control cells (all
p
≤ 0.05). In lung adenocarcinoma patients, CAV-1 expression was positively correlated with lymph node metastasis and cancer stage. Finally, CAV-1 expression was associated with the expression of Ki-67, a marker of cell proliferation. CAV-1 enhanced GLC-82 cell proliferation, migration, and invasion possibly through EGFR and ERK signaling. Furthermore, the relationship of CAV-1 with Ki67 expression, a marker of proliferative capacity, in lung adenocarcinoma samples is suggestive of its role in disease progression. Further studies are required to confirm the role of CAV-1 in the metastasis of lung adenocarcinoma as well as its potential prognostic and therapeutic value.</description><identifier>ISSN: 1357-0560</identifier><identifier>EISSN: 1559-131X</identifier><identifier>DOI: 10.1007/s12032-015-0644-5</identifier><identifier>PMID: 26094077</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Adenocarcinoma - genetics ; Adenocarcinoma - pathology ; Adenocarcinoma of Lung ; Animals ; Cancer ; Caveolin 1 - genetics ; Cell growth ; Cell Line, Tumor ; Cell Movement - genetics ; Cell Proliferation - genetics ; ErbB Receptors - genetics ; Female ; Gene Expression Regulation, Neoplastic - genetics ; Hematology ; Humans ; Internal Medicine ; Ki-67 Antigen - genetics ; Kinases ; Lung Neoplasms - genetics ; Lung Neoplasms - pathology ; Lymphatic Metastasis - genetics ; Lymphatic Metastasis - pathology ; Male ; MAP Kinase Signaling System - genetics ; Medicine ; Medicine & Public Health ; Metastasis ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Middle Aged ; Neoplasm Invasiveness - genetics ; Neoplasm Invasiveness - pathology ; Oncology ; Original Paper ; Pathology ; Phosphorylation ; Phosphorylation - genetics ; Prognosis ; Signal Transduction - genetics</subject><ispartof>Medical oncology (Northwood, London, England), 2015-07, Vol.32 (7), p.207-207, Article 207</ispartof><rights>Springer Science+Business Media New York 2015</rights><rights>Springer Science+Business Media New York 2015.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-8c413ee178359d4df8046179f34d2dba7bd19122526f6070eccdc8575aaf17c73</citedby><cites>FETCH-LOGICAL-c372t-8c413ee178359d4df8046179f34d2dba7bd19122526f6070eccdc8575aaf17c73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12032-015-0644-5$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12032-015-0644-5$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26094077$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Luan, Tian-Yan</creatorcontrib><creatorcontrib>Zhu, Tie-Nian</creatorcontrib><creatorcontrib>Cui, Yu-Jie</creatorcontrib><creatorcontrib>Zhang, Gang</creatorcontrib><creatorcontrib>Song, Xue-Jing</creatorcontrib><creatorcontrib>Gao, Dong-Mei</creatorcontrib><creatorcontrib>Zhang, Yi-Mei</creatorcontrib><creatorcontrib>Zhao, Qing-Lan</creatorcontrib><creatorcontrib>Liu, Shuang</creatorcontrib><creatorcontrib>Su, Tong-Yi</creatorcontrib><creatorcontrib>Zhao, Rui-Jing</creatorcontrib><title>Expression of caveolin-1 is correlated with lung adenocarcinoma proliferation, migration, and invasion</title><title>Medical oncology (Northwood, London, England)</title><addtitle>Med Oncol</addtitle><addtitle>Med Oncol</addtitle><description>Both tumor suppressor and tumor promoter roles, which are dependent on the tumor type, have been described for caveolin-1 (CAV-1). Because CAV-1 can modulate cell signaling, we tested the hypothesis that it regulates lung adenocarcinoma cell proliferation and metastasis via modulation of epidermal growth factor receptor (EGFR) activity. The lung adenocarcinoma cell line, GLC-82, was transfected with pcDNA3.1CAV-1 plasmid, before cell proliferation, migration, and invasion were analyzed. In the in vivo xenograft model, the relationship between the CAV-1 expression and EGFR phosphorylation and signaling was assessed by western blot analysis. The relationship between the CAV-1 as well as Ki67 expression and the clinicopathological characteristics of 68 lung adenocarcinoma patients was also examined using immunohistochemistry. Overexpression of CAV-1 significantly increased GLC-82 proliferation (
p
< 0.001), migration (
p
< 0.001), and invasion (
p
= 0.002) as well as EGFR and ERK phosphorylation (
p
< 0.05). The GLC-82/CAV-1 cell tumors were also significantly larger than those of control cells (all
p
≤ 0.05). In lung adenocarcinoma patients, CAV-1 expression was positively correlated with lymph node metastasis and cancer stage. Finally, CAV-1 expression was associated with the expression of Ki-67, a marker of cell proliferation. CAV-1 enhanced GLC-82 cell proliferation, migration, and invasion possibly through EGFR and ERK signaling. Furthermore, the relationship of CAV-1 with Ki67 expression, a marker of proliferative capacity, in lung adenocarcinoma samples is suggestive of its role in disease progression. Further studies are required to confirm the role of CAV-1 in the metastasis of lung adenocarcinoma as well as its potential prognostic and therapeutic value.</description><subject>Adenocarcinoma - genetics</subject><subject>Adenocarcinoma - pathology</subject><subject>Adenocarcinoma of Lung</subject><subject>Animals</subject><subject>Cancer</subject><subject>Caveolin 1 - genetics</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - genetics</subject><subject>Cell Proliferation - genetics</subject><subject>ErbB Receptors - genetics</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic - genetics</subject><subject>Hematology</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Ki-67 Antigen - genetics</subject><subject>Kinases</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - pathology</subject><subject>Lymphatic Metastasis - genetics</subject><subject>Lymphatic Metastasis - pathology</subject><subject>Male</subject><subject>MAP Kinase Signaling System - genetics</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Middle Aged</subject><subject>Neoplasm Invasiveness - genetics</subject><subject>Neoplasm Invasiveness - pathology</subject><subject>Oncology</subject><subject>Original Paper</subject><subject>Pathology</subject><subject>Phosphorylation</subject><subject>Phosphorylation - genetics</subject><subject>Prognosis</subject><subject>Signal Transduction - genetics</subject><issn>1357-0560</issn><issn>1559-131X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kUtr3TAQRkVoyfsHdFME3WQRtRrZsqxlCGkTCGTTQnZCV48bBVu6lew8_n1lblJCICsN6MyZYT6EvgD9DpSKHwUYbRihwAnt2pbwHbQPnEsCDdx-qnXDBaG8o3vooJR7ShlwJnfRHuuobKkQ-8hfPG2yKyWkiJPHRj-4NIRIAIeCTcrZDXpyFj-G6Q4Pc1xjbV1MRmcTYho13uTKe5f1VBWneAzr11JHi0N80Iv7CH32eiju-OU9RH9-Xvw-vyTXN7-uzs-uiWkEm0hvWmicA9E3XNrW-p62HQjpm9Yyu9JiZUECY5x1vqOCOmOs6bngWnsQRjSH6GTrrWv9nV2Z1BiKccOgo0tzUdBJqOeSfEG_vUPv05xj3W6hJAPWi7ZSsKVMTqVk59Umh1HnZwVULSGobQiqWtUSguK15-uLeV6Nzv7veL16BdgWKPUrrl1-M_pD6z-DiZIE</recordid><startdate>20150701</startdate><enddate>20150701</enddate><creator>Luan, Tian-Yan</creator><creator>Zhu, Tie-Nian</creator><creator>Cui, Yu-Jie</creator><creator>Zhang, Gang</creator><creator>Song, Xue-Jing</creator><creator>Gao, Dong-Mei</creator><creator>Zhang, Yi-Mei</creator><creator>Zhao, Qing-Lan</creator><creator>Liu, Shuang</creator><creator>Su, Tong-Yi</creator><creator>Zhao, Rui-Jing</creator><general>Springer US</general><general>Springer Nature B.V</general><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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20150701</creationdate><title>Expression of caveolin-1 is correlated with lung adenocarcinoma proliferation, migration, and invasion</title><author>Luan, Tian-Yan ; Zhu, Tie-Nian ; Cui, Yu-Jie ; Zhang, Gang ; Song, Xue-Jing ; Gao, Dong-Mei ; Zhang, Yi-Mei ; Zhao, Qing-Lan ; Liu, Shuang ; Su, Tong-Yi ; Zhao, Rui-Jing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-8c413ee178359d4df8046179f34d2dba7bd19122526f6070eccdc8575aaf17c73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Adenocarcinoma - genetics</topic><topic>Adenocarcinoma - pathology</topic><topic>Adenocarcinoma of Lung</topic><topic>Animals</topic><topic>Cancer</topic><topic>Caveolin 1 - genetics</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - genetics</topic><topic>Cell Proliferation - genetics</topic><topic>ErbB Receptors - genetics</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic - genetics</topic><topic>Hematology</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Ki-67 Antigen - genetics</topic><topic>Kinases</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - pathology</topic><topic>Lymphatic Metastasis - genetics</topic><topic>Lymphatic Metastasis - pathology</topic><topic>Male</topic><topic>MAP Kinase Signaling System - genetics</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metastasis</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>Middle Aged</topic><topic>Neoplasm Invasiveness - genetics</topic><topic>Neoplasm Invasiveness - pathology</topic><topic>Oncology</topic><topic>Original Paper</topic><topic>Pathology</topic><topic>Phosphorylation</topic><topic>Phosphorylation - genetics</topic><topic>Prognosis</topic><topic>Signal Transduction - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Luan, Tian-Yan</creatorcontrib><creatorcontrib>Zhu, Tie-Nian</creatorcontrib><creatorcontrib>Cui, Yu-Jie</creatorcontrib><creatorcontrib>Zhang, Gang</creatorcontrib><creatorcontrib>Song, Xue-Jing</creatorcontrib><creatorcontrib>Gao, Dong-Mei</creatorcontrib><creatorcontrib>Zhang, Yi-Mei</creatorcontrib><creatorcontrib>Zhao, Qing-Lan</creatorcontrib><creatorcontrib>Liu, Shuang</creatorcontrib><creatorcontrib>Su, Tong-Yi</creatorcontrib><creatorcontrib>Zhao, Rui-Jing</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Medical oncology (Northwood, London, England)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Luan, Tian-Yan</au><au>Zhu, Tie-Nian</au><au>Cui, Yu-Jie</au><au>Zhang, Gang</au><au>Song, Xue-Jing</au><au>Gao, Dong-Mei</au><au>Zhang, Yi-Mei</au><au>Zhao, Qing-Lan</au><au>Liu, Shuang</au><au>Su, Tong-Yi</au><au>Zhao, Rui-Jing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Expression of caveolin-1 is correlated with lung adenocarcinoma proliferation, migration, and invasion</atitle><jtitle>Medical oncology (Northwood, London, England)</jtitle><stitle>Med Oncol</stitle><addtitle>Med Oncol</addtitle><date>2015-07-01</date><risdate>2015</risdate><volume>32</volume><issue>7</issue><spage>207</spage><epage>207</epage><pages>207-207</pages><artnum>207</artnum><issn>1357-0560</issn><eissn>1559-131X</eissn><abstract>Both tumor suppressor and tumor promoter roles, which are dependent on the tumor type, have been described for caveolin-1 (CAV-1). Because CAV-1 can modulate cell signaling, we tested the hypothesis that it regulates lung adenocarcinoma cell proliferation and metastasis via modulation of epidermal growth factor receptor (EGFR) activity. The lung adenocarcinoma cell line, GLC-82, was transfected with pcDNA3.1CAV-1 plasmid, before cell proliferation, migration, and invasion were analyzed. In the in vivo xenograft model, the relationship between the CAV-1 expression and EGFR phosphorylation and signaling was assessed by western blot analysis. The relationship between the CAV-1 as well as Ki67 expression and the clinicopathological characteristics of 68 lung adenocarcinoma patients was also examined using immunohistochemistry. Overexpression of CAV-1 significantly increased GLC-82 proliferation (
p
< 0.001), migration (
p
< 0.001), and invasion (
p
= 0.002) as well as EGFR and ERK phosphorylation (
p
< 0.05). The GLC-82/CAV-1 cell tumors were also significantly larger than those of control cells (all
p
≤ 0.05). In lung adenocarcinoma patients, CAV-1 expression was positively correlated with lymph node metastasis and cancer stage. Finally, CAV-1 expression was associated with the expression of Ki-67, a marker of cell proliferation. CAV-1 enhanced GLC-82 cell proliferation, migration, and invasion possibly through EGFR and ERK signaling. Furthermore, the relationship of CAV-1 with Ki67 expression, a marker of proliferative capacity, in lung adenocarcinoma samples is suggestive of its role in disease progression. Further studies are required to confirm the role of CAV-1 in the metastasis of lung adenocarcinoma as well as its potential prognostic and therapeutic value.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>26094077</pmid><doi>10.1007/s12032-015-0644-5</doi><tpages>1</tpages></addata></record> |
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| ispartof | Medical oncology (Northwood, London, England), 2015-07, Vol.32 (7), p.207-207, Article 207 |
| issn | 1357-0560 1559-131X |
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| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | Adenocarcinoma - genetics Adenocarcinoma - pathology Adenocarcinoma of Lung Animals Cancer Caveolin 1 - genetics Cell growth Cell Line, Tumor Cell Movement - genetics Cell Proliferation - genetics ErbB Receptors - genetics Female Gene Expression Regulation, Neoplastic - genetics Hematology Humans Internal Medicine Ki-67 Antigen - genetics Kinases Lung Neoplasms - genetics Lung Neoplasms - pathology Lymphatic Metastasis - genetics Lymphatic Metastasis - pathology Male MAP Kinase Signaling System - genetics Medicine Medicine & Public Health Metastasis Mice Mice, Inbred BALB C Mice, Nude Middle Aged Neoplasm Invasiveness - genetics Neoplasm Invasiveness - pathology Oncology Original Paper Pathology Phosphorylation Phosphorylation - genetics Prognosis Signal Transduction - genetics |
| title | Expression of caveolin-1 is correlated with lung adenocarcinoma proliferation, migration, and invasion |
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