The Proinflammatory Cytokine, IL-6, and its Interference with bFGF Signaling and PSMA in Prostate Cancer Cells
The aim of the present work was to study the expression of the proinflammatory cytokine, interleukin-6 (IL-6), mediated by bFGF signaling and its possible crosstalk with prostate-specific membrane antigen (PSMA) in LNCaP and PC3-PSMA prostate cancer cell lines. PC3 cells stably transfected with PSMA...
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| Veröffentlicht in: | Inflammation 2013-06, Vol.36 (3), p.643-650 |
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| creator | Ben Jemaa, Awatef Sallami, Sataa Ramarli, Dunia Colombatti, Marco Oueslati, Ridha |
| description | The aim of the present work was to study the expression of the proinflammatory cytokine, interleukin-6 (IL-6), mediated by bFGF signaling and its possible crosstalk with prostate-specific membrane antigen (PSMA) in LNCaP and PC3-PSMA prostate cancer cell lines. PC3 cells stably transfected with PSMA gene were used for restoring PSMA expression. LNCaP and PC3-PSMA cells were exposed to 10 ng/mL of basic fibroblast growth factor (bFGF). IL-6 production was measured by ELISA assay, and levels of PSMA expression were assessed by flow cytometry. AKT, ERK1/2, and p38 phosphorylation were detected by Western blot. bFGF enhances IL-6 production in LNCaP and PC3-PSMA prostate cancer cells. The effect of bFGF on stimulating IL-6 secretion was greater in LNCaP than in PC3-PSMA cells. In the presence of bFGF, PSMA expression was activated after 4 days of treatment in LNCaP and PC3-PSMA cells. This activation was not maintained after long term of treatment in both metastatic cell lines. Solely MAPKs pathways (ERK1/2 and p38) were activated after bFGF stimulation in both metastatic cell lines, whereas AKT did not show any activation. The interference of the proinflammatory cytokine, IL-6, with bFGF signaling and PSMA, should be of high clinical relevance in the treatment of metastatic prostate cancer. In developing novel therapeutic modalities targeting IL-6, significant attention should be given to PSMA and its inactivation to fight against prostate cancer. |
| doi_str_mv | 10.1007/s10753-012-9586-7 |
| format | Article |
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PC3 cells stably transfected with PSMA gene were used for restoring PSMA expression. LNCaP and PC3-PSMA cells were exposed to 10 ng/mL of basic fibroblast growth factor (bFGF). IL-6 production was measured by ELISA assay, and levels of PSMA expression were assessed by flow cytometry. AKT, ERK1/2, and p38 phosphorylation were detected by Western blot. bFGF enhances IL-6 production in LNCaP and PC3-PSMA prostate cancer cells. The effect of bFGF on stimulating IL-6 secretion was greater in LNCaP than in PC3-PSMA cells. In the presence of bFGF, PSMA expression was activated after 4 days of treatment in LNCaP and PC3-PSMA cells. This activation was not maintained after long term of treatment in both metastatic cell lines. Solely MAPKs pathways (ERK1/2 and p38) were activated after bFGF stimulation in both metastatic cell lines, whereas AKT did not show any activation. The interference of the proinflammatory cytokine, IL-6, with bFGF signaling and PSMA, should be of high clinical relevance in the treatment of metastatic prostate cancer. In developing novel therapeutic modalities targeting IL-6, significant attention should be given to PSMA and its inactivation to fight against prostate cancer.</description><identifier>ISSN: 0360-3997</identifier><identifier>EISSN: 1573-2576</identifier><identifier>DOI: 10.1007/s10753-012-9586-7</identifier><identifier>PMID: 23250823</identifier><identifier>CODEN: INFLD4</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Antigens, Surface - biosynthesis ; Antigens, Surface - metabolism ; Biomedical and Life Sciences ; Biomedicine ; Cell Line, Tumor ; Extracellular Signal-Regulated MAP Kinases - metabolism ; Fibroblast Growth Factor 2 - metabolism ; Gene Expression Regulation, Neoplastic ; Glutamate Carboxypeptidase II - biosynthesis ; Glutamate Carboxypeptidase II - metabolism ; Humans ; Immunology ; Interleukin-6 - metabolism ; Internal Medicine ; Male ; p38 Mitogen-Activated Protein Kinases - metabolism ; Pathology ; Pharmacology/Toxicology ; Phosphorylation ; Prostatic Neoplasms - genetics ; Prostatic Neoplasms - immunology ; Prostatic Neoplasms - metabolism ; Proto-Oncogene Proteins c-akt - metabolism ; Rheumatology ; Signal Transduction</subject><ispartof>Inflammation, 2013-06, Vol.36 (3), p.643-650</ispartof><rights>Springer Science+Business Media New York 2012</rights><rights>Springer Science+Business Media New York 2013</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c405t-bfe1915114dd57595f5e8a4eda84957e5082deb566b9f184573291f256803fa93</citedby><cites>FETCH-LOGICAL-c405t-bfe1915114dd57595f5e8a4eda84957e5082deb566b9f184573291f256803fa93</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/s10753-012-9586-7$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10753-012-9586-7$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,777,781,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23250823$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ben Jemaa, Awatef</creatorcontrib><creatorcontrib>Sallami, Sataa</creatorcontrib><creatorcontrib>Ramarli, Dunia</creatorcontrib><creatorcontrib>Colombatti, Marco</creatorcontrib><creatorcontrib>Oueslati, Ridha</creatorcontrib><title>The Proinflammatory Cytokine, IL-6, and its Interference with bFGF Signaling and PSMA in Prostate Cancer Cells</title><title>Inflammation</title><addtitle>Inflammation</addtitle><addtitle>Inflammation</addtitle><description>The aim of the present work was to study the expression of the proinflammatory cytokine, interleukin-6 (IL-6), mediated by bFGF signaling and its possible crosstalk with prostate-specific membrane antigen (PSMA) in LNCaP and PC3-PSMA prostate cancer cell lines. PC3 cells stably transfected with PSMA gene were used for restoring PSMA expression. LNCaP and PC3-PSMA cells were exposed to 10 ng/mL of basic fibroblast growth factor (bFGF). IL-6 production was measured by ELISA assay, and levels of PSMA expression were assessed by flow cytometry. AKT, ERK1/2, and p38 phosphorylation were detected by Western blot. bFGF enhances IL-6 production in LNCaP and PC3-PSMA prostate cancer cells. The effect of bFGF on stimulating IL-6 secretion was greater in LNCaP than in PC3-PSMA cells. In the presence of bFGF, PSMA expression was activated after 4 days of treatment in LNCaP and PC3-PSMA cells. This activation was not maintained after long term of treatment in both metastatic cell lines. Solely MAPKs pathways (ERK1/2 and p38) were activated after bFGF stimulation in both metastatic cell lines, whereas AKT did not show any activation. 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PC3 cells stably transfected with PSMA gene were used for restoring PSMA expression. LNCaP and PC3-PSMA cells were exposed to 10 ng/mL of basic fibroblast growth factor (bFGF). IL-6 production was measured by ELISA assay, and levels of PSMA expression were assessed by flow cytometry. AKT, ERK1/2, and p38 phosphorylation were detected by Western blot. bFGF enhances IL-6 production in LNCaP and PC3-PSMA prostate cancer cells. The effect of bFGF on stimulating IL-6 secretion was greater in LNCaP than in PC3-PSMA cells. In the presence of bFGF, PSMA expression was activated after 4 days of treatment in LNCaP and PC3-PSMA cells. This activation was not maintained after long term of treatment in both metastatic cell lines. Solely MAPKs pathways (ERK1/2 and p38) were activated after bFGF stimulation in both metastatic cell lines, whereas AKT did not show any activation. The interference of the proinflammatory cytokine, IL-6, with bFGF signaling and PSMA, should be of high clinical relevance in the treatment of metastatic prostate cancer. In developing novel therapeutic modalities targeting IL-6, significant attention should be given to PSMA and its inactivation to fight against prostate cancer.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>23250823</pmid><doi>10.1007/s10753-012-9586-7</doi><tpages>8</tpages></addata></record> |
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| subjects | Antigens, Surface - biosynthesis Antigens, Surface - metabolism Biomedical and Life Sciences Biomedicine Cell Line, Tumor Extracellular Signal-Regulated MAP Kinases - metabolism Fibroblast Growth Factor 2 - metabolism Gene Expression Regulation, Neoplastic Glutamate Carboxypeptidase II - biosynthesis Glutamate Carboxypeptidase II - metabolism Humans Immunology Interleukin-6 - metabolism Internal Medicine Male p38 Mitogen-Activated Protein Kinases - metabolism Pathology Pharmacology/Toxicology Phosphorylation Prostatic Neoplasms - genetics Prostatic Neoplasms - immunology Prostatic Neoplasms - metabolism Proto-Oncogene Proteins c-akt - metabolism Rheumatology Signal Transduction |
| title | The Proinflammatory Cytokine, IL-6, and its Interference with bFGF Signaling and PSMA in Prostate Cancer Cells |
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