Arachidonic acid metabolism in growth control of A549 human lung adenocarcinoma cells
The role of individual eicosanoids of the arachidonic acid (AA) cascade in the growth control of A549 human lung adenocarcinoma cells has been studied. Cyclooxygenase and lipoxygenase metabolites of [14C]AA incorporated were actively synthesized in the cultures of tumor cells with full confluence un...
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| Veröffentlicht in: | Biochemistry (Moscow) 2002-09, Vol.67 (9), p.1021 |
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| creator | Kudryavtsev, I A Golenko, O D Gudkova, M V Myasishcheva, N V |
| description | The role of individual eicosanoids of the arachidonic acid (AA) cascade in the growth control of A549 human lung adenocarcinoma cells has been studied. Cyclooxygenase and lipoxygenase metabolites of [14C]AA incorporated were actively synthesized in the cultures of tumor cells with full confluence unaccomplished. In such cultures inhibitors of AA metabolism (indomethacin and esculetin) and also a lipoxygenase metabolite of AA, 15-hydroxyeicosatetraenoic acid (15-HETE), significantly suppressed the incorporation of [3H]thymidine and biosynthesis of prostaglandin E2 (PGE2). Other lipoxygenase metabolites of AA (5-HETE and 12-HETE) had no effect on these parameters. The basic fibroblast growth factor (bFGF) had practically no affect on the growth of A549 cells and the PGE2 production in cultures with 5% fetal calf serum (FCS); however, in the presence of 0.5% FCS this factor significantly increased the number of tumor cells. The growth-stimulating effect of bFGF was completely abolished by a cyclooxygenase inhibitor indomethacin. The data suggest a key role of PGE2 in the growth control of A549 cells with an active synthesis of cyclooxygenase and lipoxygenase metabolites of AA, its importance in realization of the mitogenic effect of bFGF, and specific features of 15-HETE as a down-regulator of the PGE2-dependent proliferation. |
| doi_str_mv | 10.1023/A:1020526119866 |
| format | Article |
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Cyclooxygenase and lipoxygenase metabolites of [14C]AA incorporated were actively synthesized in the cultures of tumor cells with full confluence unaccomplished. In such cultures inhibitors of AA metabolism (indomethacin and esculetin) and also a lipoxygenase metabolite of AA, 15-hydroxyeicosatetraenoic acid (15-HETE), significantly suppressed the incorporation of [3H]thymidine and biosynthesis of prostaglandin E2 (PGE2). Other lipoxygenase metabolites of AA (5-HETE and 12-HETE) had no effect on these parameters. The basic fibroblast growth factor (bFGF) had practically no affect on the growth of A549 cells and the PGE2 production in cultures with 5% fetal calf serum (FCS); however, in the presence of 0.5% FCS this factor significantly increased the number of tumor cells. The growth-stimulating effect of bFGF was completely abolished by a cyclooxygenase inhibitor indomethacin. The data suggest a key role of PGE2 in the growth control of A549 cells with an active synthesis of cyclooxygenase and lipoxygenase metabolites of AA, its importance in realization of the mitogenic effect of bFGF, and specific features of 15-HETE as a down-regulator of the PGE2-dependent proliferation.</description><identifier>ISSN: 0006-2979</identifier><identifier>EISSN: 1608-3040</identifier><identifier>DOI: 10.1023/A:1020526119866</identifier><identifier>PMID: 12387716</identifier><language>eng</language><publisher>United States: Springer Nature B.V</publisher><subject>Adenocarcinoma - metabolism ; Arachidonic Acids - metabolism ; Biosynthesis ; Carbon Radioisotopes ; Cell Division - drug effects ; Cell Division - physiology ; Cells ; Cyclooxygenase Inhibitors - pharmacology ; Dinoprost - biosynthesis ; Dinoprostone - biosynthesis ; DNA - metabolism ; Fibroblast Growth Factor 2 - pharmacology ; Humans ; Hydroxyeicosatetraenoic Acids - biosynthesis ; Hydroxyeicosatetraenoic Acids - chemistry ; Hydroxyeicosatetraenoic Acids - pharmacology ; Indomethacin - pharmacology ; Lung Neoplasms - metabolism ; Metabolites ; Thymidine - chemistry ; Thymidine - metabolism ; Tritium ; Tumor Cells, Cultured ; Umbelliferones - pharmacology</subject><ispartof>Biochemistry (Moscow), 2002-09, Vol.67 (9), p.1021</ispartof><rights>MAIK "Nauka/Interperiodica" 2002</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></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/12387716$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kudryavtsev, I A</creatorcontrib><creatorcontrib>Golenko, O D</creatorcontrib><creatorcontrib>Gudkova, M V</creatorcontrib><creatorcontrib>Myasishcheva, N V</creatorcontrib><title>Arachidonic acid metabolism in growth control of A549 human lung adenocarcinoma cells</title><title>Biochemistry (Moscow)</title><addtitle>Biochemistry (Mosc)</addtitle><description>The role of individual eicosanoids of the arachidonic acid (AA) cascade in the growth control of A549 human lung adenocarcinoma cells has been studied. Cyclooxygenase and lipoxygenase metabolites of [14C]AA incorporated were actively synthesized in the cultures of tumor cells with full confluence unaccomplished. In such cultures inhibitors of AA metabolism (indomethacin and esculetin) and also a lipoxygenase metabolite of AA, 15-hydroxyeicosatetraenoic acid (15-HETE), significantly suppressed the incorporation of [3H]thymidine and biosynthesis of prostaglandin E2 (PGE2). Other lipoxygenase metabolites of AA (5-HETE and 12-HETE) had no effect on these parameters. The basic fibroblast growth factor (bFGF) had practically no affect on the growth of A549 cells and the PGE2 production in cultures with 5% fetal calf serum (FCS); however, in the presence of 0.5% FCS this factor significantly increased the number of tumor cells. The growth-stimulating effect of bFGF was completely abolished by a cyclooxygenase inhibitor indomethacin. The data suggest a key role of PGE2 in the growth control of A549 cells with an active synthesis of cyclooxygenase and lipoxygenase metabolites of AA, its importance in realization of the mitogenic effect of bFGF, and specific features of 15-HETE as a down-regulator of the PGE2-dependent proliferation.</description><subject>Adenocarcinoma - metabolism</subject><subject>Arachidonic Acids - metabolism</subject><subject>Biosynthesis</subject><subject>Carbon Radioisotopes</subject><subject>Cell Division - drug effects</subject><subject>Cell Division - physiology</subject><subject>Cells</subject><subject>Cyclooxygenase Inhibitors - pharmacology</subject><subject>Dinoprost - biosynthesis</subject><subject>Dinoprostone - biosynthesis</subject><subject>DNA - metabolism</subject><subject>Fibroblast Growth Factor 2 - pharmacology</subject><subject>Humans</subject><subject>Hydroxyeicosatetraenoic Acids - biosynthesis</subject><subject>Hydroxyeicosatetraenoic Acids - chemistry</subject><subject>Hydroxyeicosatetraenoic Acids - pharmacology</subject><subject>Indomethacin - pharmacology</subject><subject>Lung Neoplasms - metabolism</subject><subject>Metabolites</subject><subject>Thymidine - chemistry</subject><subject>Thymidine - metabolism</subject><subject>Tritium</subject><subject>Tumor Cells, Cultured</subject><subject>Umbelliferones - pharmacology</subject><issn>0006-2979</issn><issn>1608-3040</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNo1kM9LwzAYhoMobk7P3iR4r375kqaJtzL8BQMv7lzSJN062mSmLeJ_b8F5enjh4X3hJeSWwQMD5I_l0wzIUTKmlZRnZMkkqIyDgHOyBACZoS70glwNw2GOCJpfkgVDroqCySXZlsnYfetiaC01tnW096OpY9cOPW0D3aX4Pe6pjWFMsaOxoWUuNN1PvQm0m8KOGudDtCbZNsTeUOu7brgmF43pBn9z4opsX54_12_Z5uP1fV1usiNyMWbOC5XXUir0ggtotOXaSaN945xUQnIE0SiunBEOrQdkRkiGvtZ57YwGviL3f73HFL8mP4zVIU4pzJNVgShRac1m6e4kTXXvXXVMbW_ST_V_Av8F7Wpdfw</recordid><startdate>20020901</startdate><enddate>20020901</enddate><creator>Kudryavtsev, I A</creator><creator>Golenko, O D</creator><creator>Gudkova, M V</creator><creator>Myasishcheva, N V</creator><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>3V.</scope><scope>7QL</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope></search><sort><creationdate>20020901</creationdate><title>Arachidonic acid metabolism in growth control of A549 human lung adenocarcinoma cells</title><author>Kudryavtsev, I A ; Golenko, O D ; Gudkova, M V ; Myasishcheva, N V</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p234t-de485b6682e4340f9c39d6a9efdd68463204f838da4d2ce021a4612eb95bda903</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Adenocarcinoma - metabolism</topic><topic>Arachidonic Acids - metabolism</topic><topic>Biosynthesis</topic><topic>Carbon Radioisotopes</topic><topic>Cell Division - drug effects</topic><topic>Cell Division - physiology</topic><topic>Cells</topic><topic>Cyclooxygenase Inhibitors - pharmacology</topic><topic>Dinoprost - biosynthesis</topic><topic>Dinoprostone - biosynthesis</topic><topic>DNA - metabolism</topic><topic>Fibroblast Growth Factor 2 - pharmacology</topic><topic>Humans</topic><topic>Hydroxyeicosatetraenoic Acids - biosynthesis</topic><topic>Hydroxyeicosatetraenoic Acids - chemistry</topic><topic>Hydroxyeicosatetraenoic Acids - pharmacology</topic><topic>Indomethacin - pharmacology</topic><topic>Lung Neoplasms - metabolism</topic><topic>Metabolites</topic><topic>Thymidine - chemistry</topic><topic>Thymidine - metabolism</topic><topic>Tritium</topic><topic>Tumor Cells, Cultured</topic><topic>Umbelliferones - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kudryavtsev, I A</creatorcontrib><creatorcontrib>Golenko, O D</creatorcontrib><creatorcontrib>Gudkova, M V</creatorcontrib><creatorcontrib>Myasishcheva, N V</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science 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 One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science 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 Basic</collection><jtitle>Biochemistry (Moscow)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kudryavtsev, I A</au><au>Golenko, O D</au><au>Gudkova, M V</au><au>Myasishcheva, N V</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Arachidonic acid metabolism in growth control of A549 human lung adenocarcinoma cells</atitle><jtitle>Biochemistry (Moscow)</jtitle><addtitle>Biochemistry (Mosc)</addtitle><date>2002-09-01</date><risdate>2002</risdate><volume>67</volume><issue>9</issue><spage>1021</spage><pages>1021-</pages><issn>0006-2979</issn><eissn>1608-3040</eissn><abstract>The role of individual eicosanoids of the arachidonic acid (AA) cascade in the growth control of A549 human lung adenocarcinoma cells has been studied. Cyclooxygenase and lipoxygenase metabolites of [14C]AA incorporated were actively synthesized in the cultures of tumor cells with full confluence unaccomplished. In such cultures inhibitors of AA metabolism (indomethacin and esculetin) and also a lipoxygenase metabolite of AA, 15-hydroxyeicosatetraenoic acid (15-HETE), significantly suppressed the incorporation of [3H]thymidine and biosynthesis of prostaglandin E2 (PGE2). Other lipoxygenase metabolites of AA (5-HETE and 12-HETE) had no effect on these parameters. The basic fibroblast growth factor (bFGF) had practically no affect on the growth of A549 cells and the PGE2 production in cultures with 5% fetal calf serum (FCS); however, in the presence of 0.5% FCS this factor significantly increased the number of tumor cells. The growth-stimulating effect of bFGF was completely abolished by a cyclooxygenase inhibitor indomethacin. The data suggest a key role of PGE2 in the growth control of A549 cells with an active synthesis of cyclooxygenase and lipoxygenase metabolites of AA, its importance in realization of the mitogenic effect of bFGF, and specific features of 15-HETE as a down-regulator of the PGE2-dependent proliferation.</abstract><cop>United States</cop><pub>Springer Nature B.V</pub><pmid>12387716</pmid><doi>10.1023/A:1020526119866</doi></addata></record> |
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| subjects | Adenocarcinoma - metabolism Arachidonic Acids - metabolism Biosynthesis Carbon Radioisotopes Cell Division - drug effects Cell Division - physiology Cells Cyclooxygenase Inhibitors - pharmacology Dinoprost - biosynthesis Dinoprostone - biosynthesis DNA - metabolism Fibroblast Growth Factor 2 - pharmacology Humans Hydroxyeicosatetraenoic Acids - biosynthesis Hydroxyeicosatetraenoic Acids - chemistry Hydroxyeicosatetraenoic Acids - pharmacology Indomethacin - pharmacology Lung Neoplasms - metabolism Metabolites Thymidine - chemistry Thymidine - metabolism Tritium Tumor Cells, Cultured Umbelliferones - pharmacology |
| title | Arachidonic acid metabolism in growth control of A549 human lung adenocarcinoma cells |
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