Transfection of Ovarian Cancer Cells with Tumor Necrosis Factor-α (TNF-α) Antisense mRNA Abolishes the Proliferative Response to Interleukin-1 (IL-1) but Not TNF-α
Recombinant interleukin-1 (IL-1) and tumor necrosis factor-α (TNF-α) can induce endogenous TNF-α mRNA expression and stimulate proliferation of epithelial ovarian cancer cells. In a previous report, proliferation induced by either cytokine could be partially blocked by soluble TNF-α receptor or by n...
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| Veröffentlicht in: | Gynecologic oncology 1994-04, Vol.53 (1), p.59-63 |
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| creator | Wu, S. Merkur, W.A. Wiener, J.R. Berchuck, A. Bast, R.C. Boyer, C.M. |
| description | Recombinant interleukin-1 (IL-1) and tumor necrosis factor-α (TNF-α) can induce endogenous TNF-α mRNA expression and stimulate proliferation of epithelial ovarian cancer cells. In a previous report, proliferation induced by either cytokine could be partially blocked by soluble TNF-α receptor or by neutralizing antibodies against TNF-α. In the present study, we have transfected the ovarian cancer cell line OVCA 432 with vectors that contain the TNF-α gene in the antisense or sense orientation. Antisense-transfected cells showed a 4.5- to 26-fold reduction in IL-1-induced TNF-α secretion. Similarly, the stimulation of [3H]thymidine incorporation by IL-1 but not by TNF-α was blocked by TNF-α antisense transfection. These results are consistent with a model in which the macrophage-derived cytokines IL-1 and TNF-α might stimulate endogenous production of TNF-α that in turn could stimulate proliferation of ovarian cancer cells by autocrine growth regulation. |
| doi_str_mv | 10.1006/gyno.1994.1088 |
| format | Article |
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In a previous report, proliferation induced by either cytokine could be partially blocked by soluble TNF-α receptor or by neutralizing antibodies against TNF-α. In the present study, we have transfected the ovarian cancer cell line OVCA 432 with vectors that contain the TNF-α gene in the antisense or sense orientation. Antisense-transfected cells showed a 4.5- to 26-fold reduction in IL-1-induced TNF-α secretion. Similarly, the stimulation of [3H]thymidine incorporation by IL-1 but not by TNF-α was blocked by TNF-α antisense transfection. These results are consistent with a model in which the macrophage-derived cytokines IL-1 and TNF-α might stimulate endogenous production of TNF-α that in turn could stimulate proliferation of ovarian cancer cells by autocrine growth regulation.</description><identifier>ISSN: 0090-8258</identifier><identifier>EISSN: 1095-6859</identifier><identifier>DOI: 10.1006/gyno.1994.1088</identifier><identifier>PMID: 8175024</identifier><identifier>CODEN: GYNOA3</identifier><language>eng</language><publisher>San Diego, CA: Elsevier Inc</publisher><subject>Biological and medical sciences ; Cell Division - drug effects ; Cell Division - physiology ; Female ; Female genital diseases ; Gynecology. Andrology. Obstetrics ; Humans ; Interleukin-1 - pharmacology ; Medical sciences ; Ovarian Neoplasms - genetics ; Ovarian Neoplasms - pathology ; RNA, Antisense - genetics ; RNA, Antisense - pharmacology ; RNA, Messenger - genetics ; RNA, Messenger - pharmacology ; Stimulation, Chemical ; Transfection ; Tumor Cells, Cultured - drug effects ; Tumor Necrosis Factor-alpha - biosynthesis ; Tumor Necrosis Factor-alpha - genetics ; Tumor Necrosis Factor-alpha - pharmacology ; Tumors</subject><ispartof>Gynecologic oncology, 1994-04, Vol.53 (1), p.59-63</ispartof><rights>1994 Academic Press</rights><rights>1994 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c283t-630eddeb80123a663cbcaccf99a373449c6fe5c7e0bfa4218d5f80dac55e9f703</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1006/gyno.1994.1088$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4117410$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8175024$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, S.</creatorcontrib><creatorcontrib>Merkur, W.A.</creatorcontrib><creatorcontrib>Wiener, J.R.</creatorcontrib><creatorcontrib>Berchuck, A.</creatorcontrib><creatorcontrib>Bast, R.C.</creatorcontrib><creatorcontrib>Boyer, C.M.</creatorcontrib><title>Transfection of Ovarian Cancer Cells with Tumor Necrosis Factor-α (TNF-α) Antisense mRNA Abolishes the Proliferative Response to Interleukin-1 (IL-1) but Not TNF-α</title><title>Gynecologic oncology</title><addtitle>Gynecol Oncol</addtitle><description>Recombinant interleukin-1 (IL-1) and tumor necrosis factor-α (TNF-α) can induce endogenous TNF-α mRNA expression and stimulate proliferation of epithelial ovarian cancer cells. In a previous report, proliferation induced by either cytokine could be partially blocked by soluble TNF-α receptor or by neutralizing antibodies against TNF-α. In the present study, we have transfected the ovarian cancer cell line OVCA 432 with vectors that contain the TNF-α gene in the antisense or sense orientation. Antisense-transfected cells showed a 4.5- to 26-fold reduction in IL-1-induced TNF-α secretion. Similarly, the stimulation of [3H]thymidine incorporation by IL-1 but not by TNF-α was blocked by TNF-α antisense transfection. These results are consistent with a model in which the macrophage-derived cytokines IL-1 and TNF-α might stimulate endogenous production of TNF-α that in turn could stimulate proliferation of ovarian cancer cells by autocrine growth regulation.</description><subject>Biological and medical sciences</subject><subject>Cell Division - drug effects</subject><subject>Cell Division - physiology</subject><subject>Female</subject><subject>Female genital diseases</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Interleukin-1 - pharmacology</subject><subject>Medical sciences</subject><subject>Ovarian Neoplasms - genetics</subject><subject>Ovarian Neoplasms - pathology</subject><subject>RNA, Antisense - genetics</subject><subject>RNA, Antisense - pharmacology</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - pharmacology</subject><subject>Stimulation, Chemical</subject><subject>Transfection</subject><subject>Tumor Cells, Cultured - drug effects</subject><subject>Tumor Necrosis Factor-alpha - biosynthesis</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><subject>Tumors</subject><issn>0090-8258</issn><issn>1095-6859</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1994</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kc-O0zAQhy0EWsrClRvSHNBq95Bi54_jHKuKQqWqi1blbDnOmBrSuNhO0b4Qd16EZ8JRq71xGo3m80_j-Qh5y-icUco_fHsc3Jw1TZlaIZ6RGaNNlXFRNc_JjNKGZiKvxEvyKoTvlNKCsvyKXAlWVzQvZ-T3zqshGNTRugGcgfuT8lYNsFSDRg9L7PsAv2zcw248OA9b1N4FG2CldHQ--_sHbnfbVap3sBiiDTgEhMPDdgGL1vU27DFA3CN88akz6FW0J4QHDEc3kdHBeojoexx_2CFjcLveZOwO2jHC1kU4Z78mL4zqA7651GvydfVxt_ycbe4_rZeLTaZzUcSMFxS7DluRflkozgvdaqW1aRpV1EVZNpobrHSNtDWqzJnoKiNop3RVYWNqWlyTm3Pu0bufI4YoDzbodAM1oBuDrHnJKed5AudncLpG8Gjk0duD8o-SUTmJkZMYOYmRk5j04N0leWwP2D3hFxNp_v4yV0Gr3iQt2oYnrGSsLtm0oDhjmK5wsuhl0BaTqs76JFF2zv5vg3825ax1</recordid><startdate>199404</startdate><enddate>199404</enddate><creator>Wu, S.</creator><creator>Merkur, W.A.</creator><creator>Wiener, J.R.</creator><creator>Berchuck, A.</creator><creator>Bast, R.C.</creator><creator>Boyer, C.M.</creator><general>Elsevier Inc</general><general>Elsevier</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>199404</creationdate><title>Transfection of Ovarian Cancer Cells with Tumor Necrosis Factor-α (TNF-α) Antisense mRNA Abolishes the Proliferative Response to Interleukin-1 (IL-1) but Not TNF-α</title><author>Wu, S. ; Merkur, W.A. ; Wiener, J.R. ; Berchuck, A. ; Bast, R.C. ; Boyer, C.M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c283t-630eddeb80123a663cbcaccf99a373449c6fe5c7e0bfa4218d5f80dac55e9f703</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1994</creationdate><topic>Biological and medical sciences</topic><topic>Cell Division - drug effects</topic><topic>Cell Division - physiology</topic><topic>Female</topic><topic>Female genital diseases</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Interleukin-1 - pharmacology</topic><topic>Medical sciences</topic><topic>Ovarian Neoplasms - genetics</topic><topic>Ovarian Neoplasms - pathology</topic><topic>RNA, Antisense - genetics</topic><topic>RNA, Antisense - pharmacology</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - pharmacology</topic><topic>Stimulation, Chemical</topic><topic>Transfection</topic><topic>Tumor Cells, Cultured - drug effects</topic><topic>Tumor Necrosis Factor-alpha - biosynthesis</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, S.</creatorcontrib><creatorcontrib>Merkur, W.A.</creatorcontrib><creatorcontrib>Wiener, J.R.</creatorcontrib><creatorcontrib>Berchuck, A.</creatorcontrib><creatorcontrib>Bast, R.C.</creatorcontrib><creatorcontrib>Boyer, C.M.</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>Gynecologic oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, S.</au><au>Merkur, W.A.</au><au>Wiener, J.R.</au><au>Berchuck, A.</au><au>Bast, R.C.</au><au>Boyer, C.M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Transfection of Ovarian Cancer Cells with Tumor Necrosis Factor-α (TNF-α) Antisense mRNA Abolishes the Proliferative Response to Interleukin-1 (IL-1) but Not TNF-α</atitle><jtitle>Gynecologic oncology</jtitle><addtitle>Gynecol Oncol</addtitle><date>1994-04</date><risdate>1994</risdate><volume>53</volume><issue>1</issue><spage>59</spage><epage>63</epage><pages>59-63</pages><issn>0090-8258</issn><eissn>1095-6859</eissn><coden>GYNOA3</coden><abstract>Recombinant interleukin-1 (IL-1) and tumor necrosis factor-α (TNF-α) can induce endogenous TNF-α mRNA expression and stimulate proliferation of epithelial ovarian cancer cells. In a previous report, proliferation induced by either cytokine could be partially blocked by soluble TNF-α receptor or by neutralizing antibodies against TNF-α. In the present study, we have transfected the ovarian cancer cell line OVCA 432 with vectors that contain the TNF-α gene in the antisense or sense orientation. Antisense-transfected cells showed a 4.5- to 26-fold reduction in IL-1-induced TNF-α secretion. Similarly, the stimulation of [3H]thymidine incorporation by IL-1 but not by TNF-α was blocked by TNF-α antisense transfection. These results are consistent with a model in which the macrophage-derived cytokines IL-1 and TNF-α might stimulate endogenous production of TNF-α that in turn could stimulate proliferation of ovarian cancer cells by autocrine growth regulation.</abstract><cop>San Diego, CA</cop><pub>Elsevier Inc</pub><pmid>8175024</pmid><doi>10.1006/gyno.1994.1088</doi><tpages>5</tpages></addata></record> |
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| ispartof | Gynecologic oncology, 1994-04, Vol.53 (1), p.59-63 |
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| subjects | Biological and medical sciences Cell Division - drug effects Cell Division - physiology Female Female genital diseases Gynecology. Andrology. Obstetrics Humans Interleukin-1 - pharmacology Medical sciences Ovarian Neoplasms - genetics Ovarian Neoplasms - pathology RNA, Antisense - genetics RNA, Antisense - pharmacology RNA, Messenger - genetics RNA, Messenger - pharmacology Stimulation, Chemical Transfection Tumor Cells, Cultured - drug effects Tumor Necrosis Factor-alpha - biosynthesis Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - pharmacology Tumors |
| title | Transfection of Ovarian Cancer Cells with Tumor Necrosis Factor-α (TNF-α) Antisense mRNA Abolishes the Proliferative Response to Interleukin-1 (IL-1) but Not TNF-α |
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