Restoration of fibroblast growth factor receptor 2IIIb enhances the chemosensitivity of human prostate cancer cells
Fibroblast growth factor receptor 2 (FGFR2) is thought to mediate an important signaling pathway between prostate epithelial cells and stromal cells for maintenance of homeostasis in normal prostate tissue. Abnormalities of FGFR2 have been shown in advanced prostate cancer or prostate cancer cell li...
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| Veröffentlicht in: | Oncology reports 2014-07, Vol.32 (1), p.65-70 |
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| creator | SHOJI, KOICHI TEISHIMA, JUN HAYASHI, TETSUTARO OHARA, SHINYA McKEEHAN, WALLACE L MATSUBARA, AKIO |
| description | Fibroblast growth factor receptor 2 (FGFR2) is thought to mediate an important signaling pathway between prostate epithelial cells and stromal cells for maintenance of homeostasis in normal prostate tissue. Abnormalities of FGFR2 have been shown in advanced prostate cancer or prostate cancer cell lines, and we previously demonstrated the tumor-suppressive effects of the restoration of FGFR2IIIb in prostate cancer cells. The aim of the present study was to determine whether FGFR2IIIb plays a role in the chemosensitivity of castration-resistant prostate cancer cells. A clonal line of PC-3 cells expressing FGFR2IIIb (PC-3R2IIIb) was established by transfection with an IRESneo2-expressing vector bearing FGFR2IIIb cDNA. The effects of chemotherapeutic agents (docetaxel, cisplatin, 5-fluorouracil and zoledronic acid) on cell viability and apoptosis were examined by MTT assay and western blot analysis, respectively. Expression levels of molecules that were markers of epithelial-to-mesenchymal transition and chemosensitivity-related proteins were assessed by western blot analysis. Viability of the PC-3R2IIIb cells was significantly lower than that of the control PC-3 cells transfected with the vector alone (PC-3neo), and viability was further suppressed by treatment with chemotherapeutic agents, particularly docetaxel. Induced expression of caspase-3 was evident in the PC-3R2IIIb cells and was further enhanced by treatment with docetaxel. Expression of N-cadherin, vimentin, survivin and XIAP was lower in the PC-3R2IIIb cells than that in the PC-3neo cells. In contrast, expression of p21 was higher in the PC-3R2IIIb cells than that in the control PC-3neo cells. These data indicate that restoration of FGFR2IIIb in castration-resistant prostate cancer cells may reverse some of the epithelial-to-mesenchymal cell properties characteristic of tumor cells and induce in part mesenchymal-to-epithelial transition properties. This together with enhancement of apoptotic pathways involving caspase-3 may enhance chemosensitivity particularly to docetaxel which is widely used in the treatment of castration-resistant prostate cancer. |
| doi_str_mv | 10.3892/or.2014.3200 |
| format | Article |
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Abnormalities of FGFR2 have been shown in advanced prostate cancer or prostate cancer cell lines, and we previously demonstrated the tumor-suppressive effects of the restoration of FGFR2IIIb in prostate cancer cells. The aim of the present study was to determine whether FGFR2IIIb plays a role in the chemosensitivity of castration-resistant prostate cancer cells. A clonal line of PC-3 cells expressing FGFR2IIIb (PC-3R2IIIb) was established by transfection with an IRESneo2-expressing vector bearing FGFR2IIIb cDNA. The effects of chemotherapeutic agents (docetaxel, cisplatin, 5-fluorouracil and zoledronic acid) on cell viability and apoptosis were examined by MTT assay and western blot analysis, respectively. Expression levels of molecules that were markers of epithelial-to-mesenchymal transition and chemosensitivity-related proteins were assessed by western blot analysis. Viability of the PC-3R2IIIb cells was significantly lower than that of the control PC-3 cells transfected with the vector alone (PC-3neo), and viability was further suppressed by treatment with chemotherapeutic agents, particularly docetaxel. Induced expression of caspase-3 was evident in the PC-3R2IIIb cells and was further enhanced by treatment with docetaxel. Expression of N-cadherin, vimentin, survivin and XIAP was lower in the PC-3R2IIIb cells than that in the PC-3neo cells. In contrast, expression of p21 was higher in the PC-3R2IIIb cells than that in the control PC-3neo cells. These data indicate that restoration of FGFR2IIIb in castration-resistant prostate cancer cells may reverse some of the epithelial-to-mesenchymal cell properties characteristic of tumor cells and induce in part mesenchymal-to-epithelial transition properties. This together with enhancement of apoptotic pathways involving caspase-3 may enhance chemosensitivity particularly to docetaxel which is widely used in the treatment of castration-resistant prostate cancer.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.2014.3200</identifier><identifier>PMID: 24839986</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Analysis ; Androgens ; Antineoplastic Agents - pharmacology ; Apoptosis ; Apoptosis - drug effects ; Biomarkers ; Cancer therapies ; Care and treatment ; Caspase 3 - metabolism ; Cell cycle ; Cell growth ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Cell Survival - drug effects ; chemosensitivity ; Chemotherapy ; Cloning ; docetaxel ; Epithelial-Mesenchymal Transition - drug effects ; fibroblast growth factor receptor 2IIIb ; Fibroblast growth factor receptors ; Fibroblasts ; Gene Expression Regulation, Neoplastic - drug effects ; Genetic aspects ; Genetic Vectors - genetics ; Growth factors ; Humans ; Laboratories ; Male ; Physiological aspects ; Polyclonal antibodies ; Prostate cancer ; Prostatic Neoplasms - pathology ; Prostatic Neoplasms, Castration-Resistant - genetics ; Prostatic Neoplasms, Castration-Resistant - pathology ; Protein Isoforms - genetics ; Protein Isoforms - metabolism ; Receptor, Fibroblast Growth Factor, Type 2 - genetics ; Receptor, Fibroblast Growth Factor, Type 2 - metabolism ; Stem cells ; Studies ; Transfection</subject><ispartof>Oncology reports, 2014-07, Vol.32 (1), p.65-70</ispartof><rights>Copyright © 2014, Spandidos Publications</rights><rights>COPYRIGHT 2014 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c482t-321dfb88423e2a5a6a358ae84a0f9149ed0ed79c629d8fafe7561cbb07fc38613</citedby><cites>FETCH-LOGICAL-c482t-321dfb88423e2a5a6a358ae84a0f9149ed0ed79c629d8fafe7561cbb07fc38613</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24839986$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>SHOJI, KOICHI</creatorcontrib><creatorcontrib>TEISHIMA, JUN</creatorcontrib><creatorcontrib>HAYASHI, TETSUTARO</creatorcontrib><creatorcontrib>OHARA, SHINYA</creatorcontrib><creatorcontrib>McKEEHAN, WALLACE L</creatorcontrib><creatorcontrib>MATSUBARA, AKIO</creatorcontrib><title>Restoration of fibroblast growth factor receptor 2IIIb enhances the chemosensitivity of human prostate cancer cells</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>Fibroblast growth factor receptor 2 (FGFR2) is thought to mediate an important signaling pathway between prostate epithelial cells and stromal cells for maintenance of homeostasis in normal prostate tissue. Abnormalities of FGFR2 have been shown in advanced prostate cancer or prostate cancer cell lines, and we previously demonstrated the tumor-suppressive effects of the restoration of FGFR2IIIb in prostate cancer cells. The aim of the present study was to determine whether FGFR2IIIb plays a role in the chemosensitivity of castration-resistant prostate cancer cells. A clonal line of PC-3 cells expressing FGFR2IIIb (PC-3R2IIIb) was established by transfection with an IRESneo2-expressing vector bearing FGFR2IIIb cDNA. The effects of chemotherapeutic agents (docetaxel, cisplatin, 5-fluorouracil and zoledronic acid) on cell viability and apoptosis were examined by MTT assay and western blot analysis, respectively. Expression levels of molecules that were markers of epithelial-to-mesenchymal transition and chemosensitivity-related proteins were assessed by western blot analysis. Viability of the PC-3R2IIIb cells was significantly lower than that of the control PC-3 cells transfected with the vector alone (PC-3neo), and viability was further suppressed by treatment with chemotherapeutic agents, particularly docetaxel. Induced expression of caspase-3 was evident in the PC-3R2IIIb cells and was further enhanced by treatment with docetaxel. Expression of N-cadherin, vimentin, survivin and XIAP was lower in the PC-3R2IIIb cells than that in the PC-3neo cells. In contrast, expression of p21 was higher in the PC-3R2IIIb cells than that in the control PC-3neo cells. These data indicate that restoration of FGFR2IIIb in castration-resistant prostate cancer cells may reverse some of the epithelial-to-mesenchymal cell properties characteristic of tumor cells and induce in part mesenchymal-to-epithelial transition properties. This together with enhancement of apoptotic pathways involving caspase-3 may enhance chemosensitivity particularly to docetaxel which is widely used in the treatment of castration-resistant prostate cancer.</description><subject>Analysis</subject><subject>Androgens</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Biomarkers</subject><subject>Cancer therapies</subject><subject>Care and treatment</subject><subject>Caspase 3 - metabolism</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Survival - drug effects</subject><subject>chemosensitivity</subject><subject>Chemotherapy</subject><subject>Cloning</subject><subject>docetaxel</subject><subject>Epithelial-Mesenchymal Transition - drug effects</subject><subject>fibroblast growth factor receptor 2IIIb</subject><subject>Fibroblast growth factor receptors</subject><subject>Fibroblasts</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Genetic aspects</subject><subject>Genetic Vectors - genetics</subject><subject>Growth factors</subject><subject>Humans</subject><subject>Laboratories</subject><subject>Male</subject><subject>Physiological aspects</subject><subject>Polyclonal antibodies</subject><subject>Prostate cancer</subject><subject>Prostatic Neoplasms - pathology</subject><subject>Prostatic Neoplasms, Castration-Resistant - genetics</subject><subject>Prostatic Neoplasms, Castration-Resistant - pathology</subject><subject>Protein Isoforms - genetics</subject><subject>Protein Isoforms - metabolism</subject><subject>Receptor, Fibroblast Growth Factor, Type 2 - genetics</subject><subject>Receptor, Fibroblast Growth Factor, Type 2 - metabolism</subject><subject>Stem cells</subject><subject>Studies</subject><subject>Transfection</subject><issn>1021-335X</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptks1rFjEQxhdRbK3ePEtAEA_uaz52s8mxFD9eKAii4C1ks5Nuym7ymmQr_e9NaK2tSA4Zwm-ezDwzTfOS4B0Tkr4PcUcx6XaMYvyoOSaDJC3tGHlcYkxJy1j_46h5ltIlxnTAXD5tjmgnmJSCHzfpK6Qcos4ueBQssm6MYVx0yugihl95RlabAqAIBg41oPv9fkTgZ-0NJJRnQGaGNSTwyWV35fJ1FZq3VXt0iCFlnQtS6YgMLEt63jyxeknw4vY-ab5__PDt7HN7_uXT_uz0vDWdoLlllEx2FKKjDKjuNdesFxpEp7GVpJMwYZgGaTiVk7DawtBzYsYRD9YwwQk7ad7e6JYqfm6lT7W6VCvQHsKWFOkZLq5xTAv6-h_0MmzRl-oUkYxyQYS4R13oBZTzNuSoTRVVpx3BA5dY8kLt_kOVM8HqTPBgXXl_kPDmXsIMeslzCstWZ5Iegu9uQFNsTRGsOkS36nitCFZ1GVSIqi6DqstQ8Fe3TW3jCtMd_Gf6fz9OB-0nN4V0x4RY_G8xaTHmPfsNWhK69A</recordid><startdate>20140701</startdate><enddate>20140701</enddate><creator>SHOJI, KOICHI</creator><creator>TEISHIMA, JUN</creator><creator>HAYASHI, TETSUTARO</creator><creator>OHARA, SHINYA</creator><creator>McKEEHAN, WALLACE L</creator><creator>MATSUBARA, AKIO</creator><general>D.A. 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pharmacology</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Biomarkers</topic><topic>Cancer therapies</topic><topic>Care and treatment</topic><topic>Caspase 3 - metabolism</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell Survival - drug effects</topic><topic>chemosensitivity</topic><topic>Chemotherapy</topic><topic>Cloning</topic><topic>docetaxel</topic><topic>Epithelial-Mesenchymal Transition - drug effects</topic><topic>fibroblast growth factor receptor 2IIIb</topic><topic>Fibroblast growth factor receptors</topic><topic>Fibroblasts</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Genetic aspects</topic><topic>Genetic Vectors - genetics</topic><topic>Growth factors</topic><topic>Humans</topic><topic>Laboratories</topic><topic>Male</topic><topic>Physiological aspects</topic><topic>Polyclonal antibodies</topic><topic>Prostate cancer</topic><topic>Prostatic Neoplasms - pathology</topic><topic>Prostatic Neoplasms, Castration-Resistant - genetics</topic><topic>Prostatic Neoplasms, Castration-Resistant - pathology</topic><topic>Protein Isoforms - genetics</topic><topic>Protein Isoforms - metabolism</topic><topic>Receptor, Fibroblast Growth Factor, Type 2 - genetics</topic><topic>Receptor, Fibroblast Growth Factor, Type 2 - metabolism</topic><topic>Stem cells</topic><topic>Studies</topic><topic>Transfection</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>SHOJI, KOICHI</creatorcontrib><creatorcontrib>TEISHIMA, JUN</creatorcontrib><creatorcontrib>HAYASHI, TETSUTARO</creatorcontrib><creatorcontrib>OHARA, SHINYA</creatorcontrib><creatorcontrib>McKEEHAN, WALLACE L</creatorcontrib><creatorcontrib>MATSUBARA, AKIO</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>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>British Nursing Database</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>Oncology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>SHOJI, KOICHI</au><au>TEISHIMA, JUN</au><au>HAYASHI, TETSUTARO</au><au>OHARA, SHINYA</au><au>McKEEHAN, WALLACE L</au><au>MATSUBARA, AKIO</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Restoration of fibroblast growth factor receptor 2IIIb enhances the chemosensitivity of human prostate cancer cells</atitle><jtitle>Oncology reports</jtitle><addtitle>Oncol Rep</addtitle><date>2014-07-01</date><risdate>2014</risdate><volume>32</volume><issue>1</issue><spage>65</spage><epage>70</epage><pages>65-70</pages><issn>1021-335X</issn><eissn>1791-2431</eissn><abstract>Fibroblast growth factor receptor 2 (FGFR2) is thought to mediate an important signaling pathway between prostate epithelial cells and stromal cells for maintenance of homeostasis in normal prostate tissue. Abnormalities of FGFR2 have been shown in advanced prostate cancer or prostate cancer cell lines, and we previously demonstrated the tumor-suppressive effects of the restoration of FGFR2IIIb in prostate cancer cells. The aim of the present study was to determine whether FGFR2IIIb plays a role in the chemosensitivity of castration-resistant prostate cancer cells. A clonal line of PC-3 cells expressing FGFR2IIIb (PC-3R2IIIb) was established by transfection with an IRESneo2-expressing vector bearing FGFR2IIIb cDNA. The effects of chemotherapeutic agents (docetaxel, cisplatin, 5-fluorouracil and zoledronic acid) on cell viability and apoptosis were examined by MTT assay and western blot analysis, respectively. Expression levels of molecules that were markers of epithelial-to-mesenchymal transition and chemosensitivity-related proteins were assessed by western blot analysis. Viability of the PC-3R2IIIb cells was significantly lower than that of the control PC-3 cells transfected with the vector alone (PC-3neo), and viability was further suppressed by treatment with chemotherapeutic agents, particularly docetaxel. Induced expression of caspase-3 was evident in the PC-3R2IIIb cells and was further enhanced by treatment with docetaxel. Expression of N-cadherin, vimentin, survivin and XIAP was lower in the PC-3R2IIIb cells than that in the PC-3neo cells. In contrast, expression of p21 was higher in the PC-3R2IIIb cells than that in the control PC-3neo cells. These data indicate that restoration of FGFR2IIIb in castration-resistant prostate cancer cells may reverse some of the epithelial-to-mesenchymal cell properties characteristic of tumor cells and induce in part mesenchymal-to-epithelial transition properties. This together with enhancement of apoptotic pathways involving caspase-3 may enhance chemosensitivity particularly to docetaxel which is widely used in the treatment of castration-resistant prostate cancer.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>24839986</pmid><doi>10.3892/or.2014.3200</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Oncology reports, 2014-07, Vol.32 (1), p.65-70 |
| issn | 1021-335X 1791-2431 |
| language | eng |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Analysis Androgens Antineoplastic Agents - pharmacology Apoptosis Apoptosis - drug effects Biomarkers Cancer therapies Care and treatment Caspase 3 - metabolism Cell cycle Cell growth Cell Line, Tumor Cell Proliferation - drug effects Cell Survival - drug effects chemosensitivity Chemotherapy Cloning docetaxel Epithelial-Mesenchymal Transition - drug effects fibroblast growth factor receptor 2IIIb Fibroblast growth factor receptors Fibroblasts Gene Expression Regulation, Neoplastic - drug effects Genetic aspects Genetic Vectors - genetics Growth factors Humans Laboratories Male Physiological aspects Polyclonal antibodies Prostate cancer Prostatic Neoplasms - pathology Prostatic Neoplasms, Castration-Resistant - genetics Prostatic Neoplasms, Castration-Resistant - pathology Protein Isoforms - genetics Protein Isoforms - metabolism Receptor, Fibroblast Growth Factor, Type 2 - genetics Receptor, Fibroblast Growth Factor, Type 2 - metabolism Stem cells Studies Transfection |
| title | Restoration of fibroblast growth factor receptor 2IIIb enhances the chemosensitivity of human prostate cancer cells |
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