Prostaglandin E2 and F2α inhibit growth of human gastric carcinoma cell line KATO III with simultaneous stimulation of cyclic AMP production
The effects of prostaglandins (PGs) on the growth of human gastric carcinoma cell line KATO III were investigated. PGE2 as well as PGF2 alpha significantly and dose-dependently inhibited the growth of this gastric carcinoma cell line (PGE2 greater than PGF2 alpha). This inhibition of cell growth by...
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| Veröffentlicht in: | Life sciences (1973) 1989, Vol.44 (1), p.75-80 |
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| container_title | Life sciences (1973) |
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| creator | NAKAMURA, A CHIBA, T YAMATANI, T YAMAGUCHI, A INUI, T MORISHITA, T KADOWAKI, S FUJITA, T |
| description | The effects of prostaglandins (PGs) on the growth of human gastric carcinoma cell line KATO III were investigated. PGE2 as well as PGF2 alpha significantly and dose-dependently inhibited the growth of this gastric carcinoma cell line (PGE2 greater than PGF2 alpha). This inhibition of cell growth by the PGs was associated with the increase in cyclic AMP production (PGE2 greater than PGF2 alpha), whereas inositol-phospholipid turnover was not affected by either PGE2 or PGF2 alpha as assessed by the formation of 3H-inositol phosphates. Furthermore, the proliferation of these gastric carcinoma cells was also suppressed by the administration of forskolin as well as of dibutyryl cyclic AMP. These results suggest that PGE2 and PGF2 alpha inhibit the growth of cultured human gastric carcinoma cells KATO III via stimulation of cyclic AMP production. |
| doi_str_mv | 10.1016/0024-3205(89)90220-8 |
| format | Article |
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PGE2 as well as PGF2 alpha significantly and dose-dependently inhibited the growth of this gastric carcinoma cell line (PGE2 greater than PGF2 alpha). This inhibition of cell growth by the PGs was associated with the increase in cyclic AMP production (PGE2 greater than PGF2 alpha), whereas inositol-phospholipid turnover was not affected by either PGE2 or PGF2 alpha as assessed by the formation of 3H-inositol phosphates. Furthermore, the proliferation of these gastric carcinoma cells was also suppressed by the administration of forskolin as well as of dibutyryl cyclic AMP. 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PGE2 as well as PGF2 alpha significantly and dose-dependently inhibited the growth of this gastric carcinoma cell line (PGE2 greater than PGF2 alpha). This inhibition of cell growth by the PGs was associated with the increase in cyclic AMP production (PGE2 greater than PGF2 alpha), whereas inositol-phospholipid turnover was not affected by either PGE2 or PGF2 alpha as assessed by the formation of 3H-inositol phosphates. Furthermore, the proliferation of these gastric carcinoma cells was also suppressed by the administration of forskolin as well as of dibutyryl cyclic AMP. These results suggest that PGE2 and PGF2 alpha inhibit the growth of cultured human gastric carcinoma cells KATO III via stimulation of cyclic AMP production.</description><subject>Biological and medical sciences</subject><subject>Bucladesine - pharmacology</subject><subject>Carcinoma - pathology</subject><subject>Cell Division - drug effects</subject><subject>Colforsin - pharmacology</subject><subject>Cyclic AMP - biosynthesis</subject><subject>Depression, Chemical</subject><subject>Dinoprost - pharmacology</subject><subject>Dinoprostone - pharmacology</subject><subject>General aspects (metabolism, cell proliferation, established cell line...)</subject><subject>Humans</subject><subject>Inositol Phosphates - biosynthesis</subject><subject>Medical sciences</subject><subject>Stomach Neoplasms - pathology</subject><subject>Tumor cell</subject><subject>Tumor Cells, Cultured</subject><subject>Tumors</subject><issn>0024-3205</issn><issn>1879-0631</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1989</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9UU1u1DAUtiqqMpTeACQvUAWLwPNPYns5qloYUdQuytpyHGfGKHGK7ajqIThML8KZcJjRrPz8vh_7fQ-hdwQ-EyDNFwDKK0ah_ijVJwWUQiVP0IpIoSpoGHmFVkfKa_QmpV8AUNeCnaEzWrOG13SF_tzHKWWzHUzofMDXFJcC39C_L9iHnW99xts4PeUdnnq8m0cT8NakHL3F1kTrwzQabN0w4MEHh7-vH-7wZrPBT75Ikh_nIZvgpjnhlJebyX4Ki5d9tkMxWf-4x49x6ma7AG_RaW-G5C4O5zn6eXP9cPWtur37urla31aW8iZXgrYCFOdCAJC2Y1JJ1pYmIWChbq3hvaJWNE4wSztQPa2NaVtaOo5w59g5utz7lqd_zy5lPfq0TLH_qxZSMg6qKUS-J9oSU4qu14_RjyY-awJ62YJeItZLxFoq_X8LWhbZ-4P_3I6uO4oOsRf8wwE3yZqhjyZYn440QYiiXLF_OVOQmg</recordid><startdate>1989</startdate><enddate>1989</enddate><creator>NAKAMURA, A</creator><creator>CHIBA, T</creator><creator>YAMATANI, T</creator><creator>YAMAGUCHI, A</creator><creator>INUI, T</creator><creator>MORISHITA, T</creator><creator>KADOWAKI, S</creator><creator>FUJITA, T</creator><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>1989</creationdate><title>Prostaglandin E2 and F2α inhibit growth of human gastric carcinoma cell line KATO III with simultaneous stimulation of cyclic AMP production</title><author>NAKAMURA, A ; CHIBA, T ; YAMATANI, T ; YAMAGUCHI, A ; INUI, T ; MORISHITA, T ; KADOWAKI, S ; FUJITA, T</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c246t-72b7094477001bd38983b72b110c05bca4f92c76e73c2d09f25aabb276ee14ee3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1989</creationdate><topic>Biological and medical sciences</topic><topic>Bucladesine - pharmacology</topic><topic>Carcinoma - pathology</topic><topic>Cell Division - drug effects</topic><topic>Colforsin - pharmacology</topic><topic>Cyclic AMP - biosynthesis</topic><topic>Depression, Chemical</topic><topic>Dinoprost - pharmacology</topic><topic>Dinoprostone - pharmacology</topic><topic>General aspects (metabolism, cell proliferation, established cell line...)</topic><topic>Humans</topic><topic>Inositol Phosphates - biosynthesis</topic><topic>Medical sciences</topic><topic>Stomach Neoplasms - pathology</topic><topic>Tumor cell</topic><topic>Tumor Cells, Cultured</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>NAKAMURA, A</creatorcontrib><creatorcontrib>CHIBA, T</creatorcontrib><creatorcontrib>YAMATANI, T</creatorcontrib><creatorcontrib>YAMAGUCHI, A</creatorcontrib><creatorcontrib>INUI, T</creatorcontrib><creatorcontrib>MORISHITA, T</creatorcontrib><creatorcontrib>KADOWAKI, S</creatorcontrib><creatorcontrib>FUJITA, T</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>Life sciences (1973)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>NAKAMURA, A</au><au>CHIBA, T</au><au>YAMATANI, T</au><au>YAMAGUCHI, A</au><au>INUI, T</au><au>MORISHITA, T</au><au>KADOWAKI, S</au><au>FUJITA, T</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Prostaglandin E2 and F2α inhibit growth of human gastric carcinoma cell line KATO III with simultaneous stimulation of cyclic AMP production</atitle><jtitle>Life sciences (1973)</jtitle><addtitle>Life Sci</addtitle><date>1989</date><risdate>1989</risdate><volume>44</volume><issue>1</issue><spage>75</spage><epage>80</epage><pages>75-80</pages><issn>0024-3205</issn><eissn>1879-0631</eissn><coden>LIFSAK</coden><abstract>The effects of prostaglandins (PGs) on the growth of human gastric carcinoma cell line KATO III were investigated. PGE2 as well as PGF2 alpha significantly and dose-dependently inhibited the growth of this gastric carcinoma cell line (PGE2 greater than PGF2 alpha). This inhibition of cell growth by the PGs was associated with the increase in cyclic AMP production (PGE2 greater than PGF2 alpha), whereas inositol-phospholipid turnover was not affected by either PGE2 or PGF2 alpha as assessed by the formation of 3H-inositol phosphates. Furthermore, the proliferation of these gastric carcinoma cells was also suppressed by the administration of forskolin as well as of dibutyryl cyclic AMP. These results suggest that PGE2 and PGF2 alpha inhibit the growth of cultured human gastric carcinoma cells KATO III via stimulation of cyclic AMP production.</abstract><cop>Amsterdam</cop><pub>Elsevier</pub><pmid>2536452</pmid><doi>10.1016/0024-3205(89)90220-8</doi><tpages>6</tpages></addata></record> |
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| ispartof | Life sciences (1973), 1989, Vol.44 (1), p.75-80 |
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| subjects | Biological and medical sciences Bucladesine - pharmacology Carcinoma - pathology Cell Division - drug effects Colforsin - pharmacology Cyclic AMP - biosynthesis Depression, Chemical Dinoprost - pharmacology Dinoprostone - pharmacology General aspects (metabolism, cell proliferation, established cell line...) Humans Inositol Phosphates - biosynthesis Medical sciences Stomach Neoplasms - pathology Tumor cell Tumor Cells, Cultured Tumors |
| title | Prostaglandin E2 and F2α inhibit growth of human gastric carcinoma cell line KATO III with simultaneous stimulation of cyclic AMP production |
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