All-trans-retinoic acid blocks cell cycle progression of human ovarian adenocarcinoma cells at late G1
We prepared single cell clones from two ovarian carcinoma cell lines, CA-OV3 and SK-OV3, and analyzed the effect of all-trans-RA treatment on cell division, DNA synthesis, and cell cycle stage distribution of these single cell clones. Our results show that despite the well-known heterogeneous nature...
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| Veröffentlicht in: | Experimental cell research 1997-05, Vol.232 (2), p.277-286 |
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| creator | Wu, S Donigan, A Platsoucas, C D Jung, W Soprano, D R Soprano, K J |
| description | We prepared single cell clones from two ovarian carcinoma cell lines, CA-OV3 and SK-OV3, and analyzed the effect of all-trans-RA treatment on cell division, DNA synthesis, and cell cycle stage distribution of these single cell clones. Our results show that despite the well-known heterogeneous nature of these cell lines, all single cell clones of SK-OV3 cells are resistant to the growth inhibitory effects of all-trans-RA. In contrast, all single cell clones of CA-OV3 cells were growth inhibited by all-trans-RA. However, the extent of growth inhibition did vary somewhat from clone to clone. Additional studies employing flow cytometry showed that all-trans-RA blocked CA-OV3 cell cycle progression in the G1 stage. Finally, all-trans-RA was able to inhibit G1 progression in growth-arrested CA-OV3 cells following stimulation with fetal bovine serum, insulin, IGF-1, or estrogen. Since each of these growth factors is known to act via distinct signal transduction pathways, our results suggest that all-trans-RA blocks G1 progression by targeting a downstream process or event which occurs at a point after the insulin/IGF-1, estrogen, and serum signal transduction pathways converge. |
| doi_str_mv | 10.1006/excr.1997.3495 |
| format | Article |
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Our results show that despite the well-known heterogeneous nature of these cell lines, all single cell clones of SK-OV3 cells are resistant to the growth inhibitory effects of all-trans-RA. In contrast, all single cell clones of CA-OV3 cells were growth inhibited by all-trans-RA. However, the extent of growth inhibition did vary somewhat from clone to clone. Additional studies employing flow cytometry showed that all-trans-RA blocked CA-OV3 cell cycle progression in the G1 stage. Finally, all-trans-RA was able to inhibit G1 progression in growth-arrested CA-OV3 cells following stimulation with fetal bovine serum, insulin, IGF-1, or estrogen. Since each of these growth factors is known to act via distinct signal transduction pathways, our results suggest that all-trans-RA blocks G1 progression by targeting a downstream process or event which occurs at a point after the insulin/IGF-1, estrogen, and serum signal transduction pathways converge.</description><identifier>ISSN: 0014-4827</identifier><identifier>DOI: 10.1006/excr.1997.3495</identifier><identifier>PMID: 9168803</identifier><language>eng</language><publisher>United States</publisher><subject>Adenocarcinoma - pathology ; Animals ; Antineoplastic Agents - pharmacology ; Cattle ; Cell Division - drug effects ; DNA Replication - drug effects ; DNA, Neoplasm - biosynthesis ; Estradiol - pharmacology ; Female ; Fetal Blood - physiology ; G1 Phase - drug effects ; Growth Inhibitors - pharmacology ; Humans ; Insulin - pharmacology ; Insulin-Like Growth Factor I - pharmacology ; Neoplasm Proteins - biosynthesis ; Neoplasm Proteins - genetics ; Ovarian Neoplasms - pathology ; RNA, Messenger - biosynthesis ; RNA, Messenger - genetics ; RNA, Neoplasm - biosynthesis ; RNA, Neoplasm - genetics ; Signal Transduction - drug effects ; Transforming Growth Factor beta - biosynthesis ; Transforming Growth Factor beta - genetics ; Tretinoin - pharmacology ; Tumor Cells, Cultured - drug effects</subject><ispartof>Experimental cell research, 1997-05, Vol.232 (2), p.277-286</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c205t-a3ccdfacbce9eb206c147f2abbff3268f5bd244aff23a779a5308924b42aa5fe3</citedby><cites>FETCH-LOGICAL-c205t-a3ccdfacbce9eb206c147f2abbff3268f5bd244aff23a779a5308924b42aa5fe3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9168803$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, S</creatorcontrib><creatorcontrib>Donigan, A</creatorcontrib><creatorcontrib>Platsoucas, C D</creatorcontrib><creatorcontrib>Jung, W</creatorcontrib><creatorcontrib>Soprano, D R</creatorcontrib><creatorcontrib>Soprano, K J</creatorcontrib><title>All-trans-retinoic acid blocks cell cycle progression of human ovarian adenocarcinoma cells at late G1</title><title>Experimental cell research</title><addtitle>Exp Cell Res</addtitle><description>We prepared single cell clones from two ovarian carcinoma cell lines, CA-OV3 and SK-OV3, and analyzed the effect of all-trans-RA treatment on cell division, DNA synthesis, and cell cycle stage distribution of these single cell clones. Our results show that despite the well-known heterogeneous nature of these cell lines, all single cell clones of SK-OV3 cells are resistant to the growth inhibitory effects of all-trans-RA. In contrast, all single cell clones of CA-OV3 cells were growth inhibited by all-trans-RA. However, the extent of growth inhibition did vary somewhat from clone to clone. Additional studies employing flow cytometry showed that all-trans-RA blocked CA-OV3 cell cycle progression in the G1 stage. Finally, all-trans-RA was able to inhibit G1 progression in growth-arrested CA-OV3 cells following stimulation with fetal bovine serum, insulin, IGF-1, or estrogen. Since each of these growth factors is known to act via distinct signal transduction pathways, our results suggest that all-trans-RA blocks G1 progression by targeting a downstream process or event which occurs at a point after the insulin/IGF-1, estrogen, and serum signal transduction pathways converge.</description><subject>Adenocarcinoma - pathology</subject><subject>Animals</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Cattle</subject><subject>Cell Division - drug effects</subject><subject>DNA Replication - drug effects</subject><subject>DNA, Neoplasm - biosynthesis</subject><subject>Estradiol - pharmacology</subject><subject>Female</subject><subject>Fetal Blood - physiology</subject><subject>G1 Phase - drug effects</subject><subject>Growth Inhibitors - pharmacology</subject><subject>Humans</subject><subject>Insulin - pharmacology</subject><subject>Insulin-Like Growth Factor I - pharmacology</subject><subject>Neoplasm Proteins - biosynthesis</subject><subject>Neoplasm Proteins - genetics</subject><subject>Ovarian Neoplasms - pathology</subject><subject>RNA, Messenger - biosynthesis</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Neoplasm - biosynthesis</subject><subject>RNA, Neoplasm - genetics</subject><subject>Signal Transduction - drug effects</subject><subject>Transforming Growth Factor beta - biosynthesis</subject><subject>Transforming Growth Factor beta - genetics</subject><subject>Tretinoin - pharmacology</subject><subject>Tumor Cells, Cultured - drug effects</subject><issn>0014-4827</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kD1PwzAYhD2ASimsbEie2BL8lQ-PVQUFqRILzNZrx4aAExc7QfDvSWjFdDfcnU4PQleU5JSQ8tZ-m5hTKaucC1mcoCUhVGSiZtUZOk_pnRBS17RcoIWkZV0TvkRu7X02ROhTFu3Q9qE1GEzbYO2D-UjYWO-x-THe4n0Mr9Gm1IYeB4ffxg4m8wWxnRQa2wcD0UwTHfzVEoYBexgs3tILdOrAJ3t51BV6ub973jxku6ft42a9ywwjxZABN6ZxYLSx0mpGSkNF5Rho7RxnZe0K3TAhwDnGoaokFJzUkgktGEDhLF-hm8PudPZztGlQXZvmM9DbMCZVScKpKKopmB-CJoaUonVqH9sO4o-iRM0w1QxTzTDVDHMqXB-XR93Z5j9-JMl_Ab7_dNM</recordid><startdate>19970501</startdate><enddate>19970501</enddate><creator>Wu, S</creator><creator>Donigan, A</creator><creator>Platsoucas, C D</creator><creator>Jung, W</creator><creator>Soprano, D R</creator><creator>Soprano, K J</creator><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>19970501</creationdate><title>All-trans-retinoic acid blocks cell cycle progression of human ovarian adenocarcinoma cells at late G1</title><author>Wu, S ; Donigan, A ; Platsoucas, C D ; Jung, W ; Soprano, D R ; Soprano, K J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c205t-a3ccdfacbce9eb206c147f2abbff3268f5bd244aff23a779a5308924b42aa5fe3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Adenocarcinoma - pathology</topic><topic>Animals</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Cattle</topic><topic>Cell Division - drug effects</topic><topic>DNA Replication - drug effects</topic><topic>DNA, Neoplasm - biosynthesis</topic><topic>Estradiol - pharmacology</topic><topic>Female</topic><topic>Fetal Blood - physiology</topic><topic>G1 Phase - drug effects</topic><topic>Growth Inhibitors - pharmacology</topic><topic>Humans</topic><topic>Insulin - pharmacology</topic><topic>Insulin-Like Growth Factor I - pharmacology</topic><topic>Neoplasm Proteins - biosynthesis</topic><topic>Neoplasm Proteins - genetics</topic><topic>Ovarian Neoplasms - pathology</topic><topic>RNA, Messenger - biosynthesis</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Neoplasm - biosynthesis</topic><topic>RNA, Neoplasm - genetics</topic><topic>Signal Transduction - drug effects</topic><topic>Transforming Growth Factor beta - biosynthesis</topic><topic>Transforming Growth Factor beta - genetics</topic><topic>Tretinoin - pharmacology</topic><topic>Tumor Cells, Cultured - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, S</creatorcontrib><creatorcontrib>Donigan, A</creatorcontrib><creatorcontrib>Platsoucas, C D</creatorcontrib><creatorcontrib>Jung, W</creatorcontrib><creatorcontrib>Soprano, D R</creatorcontrib><creatorcontrib>Soprano, K J</creatorcontrib><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>Experimental cell research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, S</au><au>Donigan, A</au><au>Platsoucas, C D</au><au>Jung, W</au><au>Soprano, D R</au><au>Soprano, K J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>All-trans-retinoic acid blocks cell cycle progression of human ovarian adenocarcinoma cells at late G1</atitle><jtitle>Experimental cell research</jtitle><addtitle>Exp Cell Res</addtitle><date>1997-05-01</date><risdate>1997</risdate><volume>232</volume><issue>2</issue><spage>277</spage><epage>286</epage><pages>277-286</pages><issn>0014-4827</issn><abstract>We prepared single cell clones from two ovarian carcinoma cell lines, CA-OV3 and SK-OV3, and analyzed the effect of all-trans-RA treatment on cell division, DNA synthesis, and cell cycle stage distribution of these single cell clones. Our results show that despite the well-known heterogeneous nature of these cell lines, all single cell clones of SK-OV3 cells are resistant to the growth inhibitory effects of all-trans-RA. In contrast, all single cell clones of CA-OV3 cells were growth inhibited by all-trans-RA. However, the extent of growth inhibition did vary somewhat from clone to clone. Additional studies employing flow cytometry showed that all-trans-RA blocked CA-OV3 cell cycle progression in the G1 stage. Finally, all-trans-RA was able to inhibit G1 progression in growth-arrested CA-OV3 cells following stimulation with fetal bovine serum, insulin, IGF-1, or estrogen. Since each of these growth factors is known to act via distinct signal transduction pathways, our results suggest that all-trans-RA blocks G1 progression by targeting a downstream process or event which occurs at a point after the insulin/IGF-1, estrogen, and serum signal transduction pathways converge.</abstract><cop>United States</cop><pmid>9168803</pmid><doi>10.1006/excr.1997.3495</doi><tpages>10</tpages></addata></record> |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Adenocarcinoma - pathology Animals Antineoplastic Agents - pharmacology Cattle Cell Division - drug effects DNA Replication - drug effects DNA, Neoplasm - biosynthesis Estradiol - pharmacology Female Fetal Blood - physiology G1 Phase - drug effects Growth Inhibitors - pharmacology Humans Insulin - pharmacology Insulin-Like Growth Factor I - pharmacology Neoplasm Proteins - biosynthesis Neoplasm Proteins - genetics Ovarian Neoplasms - pathology RNA, Messenger - biosynthesis RNA, Messenger - genetics RNA, Neoplasm - biosynthesis RNA, Neoplasm - genetics Signal Transduction - drug effects Transforming Growth Factor beta - biosynthesis Transforming Growth Factor beta - genetics Tretinoin - pharmacology Tumor Cells, Cultured - drug effects |
| title | All-trans-retinoic acid blocks cell cycle progression of human ovarian adenocarcinoma cells at late G1 |
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