Modulation of IGF-2 expression during growth and differentiation of human neuroblastoma cells: Retinoic acid may induce IGF-2
Insulin-like growth factor 2 (IGF-2) is the major autocrine growth factor for neuroblastoma. IGF-2 mRNA can just be detected in SK-N-BE(2) cell line; higher levels are present in two clones derived from it [BE(2)-C; BE(2)-M17]. IGF-2 mRNA is increased by retinoic acid (RA) only in the clones. IGF-2...
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| Veröffentlicht in: | Neuroscience letters 1993-03, Vol.151 (2), p.187-191 |
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| container_title | Neuroscience letters |
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| creator | Melino, Gerry Stephanou, Anastasis Annicchiarico-Petruzzelli, Margherita Knight, Richard A. Finazzi-Agro, Alessandro Lightman, Stafford L. |
| description | Insulin-like growth factor 2 (IGF-2) is the major autocrine growth factor for neuroblastoma. IGF-2 mRNA can just be detected in SK-N-BE(2) cell line; higher levels are present in two clones derived from it [BE(2)-C; BE(2)-M17]. IGF-2 mRNA is increased by retinoic acid (RA) only in the clones. IGF-2 expression/induction is more marked in BE(2)-M17, which shows more RA-resistance (evaluated as growth inhibition, neurite outgrowth and induction of programmed cell death). Under RA exposure, the parental line shows a more pronounced growth inhibition, neurite outgrowth and programmed cell death, as compared to its clones. BE(2)-C cells also express type 1 IGF receptor mRNA, though with a different time course than for expression of IGF-2. The data suggest that IGF-2 expression is correlated with growth, and may counteract the growth retardation, neurite outgrowth and programmed cell death effects of retinoic acid. Therefore the autocrine pattern of IGF-2 production by neuroblastoma cells may promote RA-resistance. |
| doi_str_mv | 10.1016/0304-3940(93)90017-F |
| format | Article |
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IGF-2 mRNA can just be detected in SK-N-BE(2) cell line; higher levels are present in two clones derived from it [BE(2)-C; BE(2)-M17]. IGF-2 mRNA is increased by retinoic acid (RA) only in the clones. IGF-2 expression/induction is more marked in BE(2)-M17, which shows more RA-resistance (evaluated as growth inhibition, neurite outgrowth and induction of programmed cell death). Under RA exposure, the parental line shows a more pronounced growth inhibition, neurite outgrowth and programmed cell death, as compared to its clones. BE(2)-C cells also express type 1 IGF receptor mRNA, though with a different time course than for expression of IGF-2. The data suggest that IGF-2 expression is correlated with growth, and may counteract the growth retardation, neurite outgrowth and programmed cell death effects of retinoic acid. Therefore the autocrine pattern of IGF-2 production by neuroblastoma cells may promote RA-resistance.</description><identifier>ISSN: 0304-3940</identifier><identifier>EISSN: 1872-7972</identifier><identifier>DOI: 10.1016/0304-3940(93)90017-F</identifier><identifier>PMID: 8506078</identifier><language>eng</language><publisher>Ireland: Elsevier Ireland Ltd</publisher><subject>Apoptosis ; Brain Neoplasms - metabolism ; Cell Differentiation - drug effects ; Cell Movement - drug effects ; Differentiation ; GHRH ; Growth Hormone - biosynthesis ; Humans ; IGF-2 ; Indicators and Reagents ; Insulin-Like Growth Factor II - biosynthesis ; Neurites - drug effects ; Neuroblastoma ; Neuroblastoma - metabolism ; Programmed cell death ; Retinoić acid ; RNA, Messenger - biosynthesis ; Tretinoin - pharmacology ; Tumor Cells, Cultured</subject><ispartof>Neuroscience letters, 1993-03, Vol.151 (2), p.187-191</ispartof><rights>1993</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c388t-71f14ac69000da3f1ec5df1431dbb3bade61c61f8a34ee7b7117ef52c00f50343</citedby><cites>FETCH-LOGICAL-c388t-71f14ac69000da3f1ec5df1431dbb3bade61c61f8a34ee7b7117ef52c00f50343</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/030439409390017F$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8506078$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Melino, Gerry</creatorcontrib><creatorcontrib>Stephanou, Anastasis</creatorcontrib><creatorcontrib>Annicchiarico-Petruzzelli, Margherita</creatorcontrib><creatorcontrib>Knight, Richard A.</creatorcontrib><creatorcontrib>Finazzi-Agro, Alessandro</creatorcontrib><creatorcontrib>Lightman, Stafford L.</creatorcontrib><title>Modulation of IGF-2 expression during growth and differentiation of human neuroblastoma cells: Retinoic acid may induce IGF-2</title><title>Neuroscience letters</title><addtitle>Neurosci Lett</addtitle><description>Insulin-like growth factor 2 (IGF-2) is the major autocrine growth factor for neuroblastoma. IGF-2 mRNA can just be detected in SK-N-BE(2) cell line; higher levels are present in two clones derived from it [BE(2)-C; BE(2)-M17]. IGF-2 mRNA is increased by retinoic acid (RA) only in the clones. IGF-2 expression/induction is more marked in BE(2)-M17, which shows more RA-resistance (evaluated as growth inhibition, neurite outgrowth and induction of programmed cell death). Under RA exposure, the parental line shows a more pronounced growth inhibition, neurite outgrowth and programmed cell death, as compared to its clones. BE(2)-C cells also express type 1 IGF receptor mRNA, though with a different time course than for expression of IGF-2. The data suggest that IGF-2 expression is correlated with growth, and may counteract the growth retardation, neurite outgrowth and programmed cell death effects of retinoic acid. Therefore the autocrine pattern of IGF-2 production by neuroblastoma cells may promote RA-resistance.</description><subject>Apoptosis</subject><subject>Brain Neoplasms - metabolism</subject><subject>Cell Differentiation - drug effects</subject><subject>Cell Movement - drug effects</subject><subject>Differentiation</subject><subject>GHRH</subject><subject>Growth Hormone - biosynthesis</subject><subject>Humans</subject><subject>IGF-2</subject><subject>Indicators and Reagents</subject><subject>Insulin-Like Growth Factor II - biosynthesis</subject><subject>Neurites - drug effects</subject><subject>Neuroblastoma</subject><subject>Neuroblastoma - metabolism</subject><subject>Programmed cell death</subject><subject>Retinoić acid</subject><subject>RNA, Messenger - biosynthesis</subject><subject>Tretinoin - pharmacology</subject><subject>Tumor Cells, Cultured</subject><issn>0304-3940</issn><issn>1872-7972</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFUU1v1DAQtRBVWQr_ACSfUDkEZuIkTjggoYotlYqQEJwtxx63Rom92Amlh_53Ena1RziN9Oa9-XiPsRcIbxCweQsCqkJ0FZx34nUHgLLYPmIbbGVZyE6Wj9nmSHnCnub8AwBqrKtTdtrW0IBsN-zhc7TzoCcfA4-OX11ui5LT712inFfMzsmHG36T4t10y3Ww3HrnKFGY_FF1O4868EBziv2g8xRHzQ0NQ37Hv9LkQ_SGa-MtH_U998HOhvabnrETp4dMzw_1jH3ffvx28am4_nJ5dfHhujCibadCosNKm2Z5EqwWDsnUdoEE2r4XvbbUoGnQtVpURLKXiJJcXRoAV4OoxBl7tZ-7S_HnTHlSo8_rhTpQnLOStWzLRpT_JWJTtwIlLMRqTzQp5pzIqV3yo073CkGt8ajVe7V6rzqh_sajtovs5WH-3I9kj6JDHkv__b5Pixu_PCWVjadgyPpEZlI2-n8v-AM3up-p</recordid><startdate>19930319</startdate><enddate>19930319</enddate><creator>Melino, Gerry</creator><creator>Stephanou, Anastasis</creator><creator>Annicchiarico-Petruzzelli, Margherita</creator><creator>Knight, Richard A.</creator><creator>Finazzi-Agro, Alessandro</creator><creator>Lightman, Stafford L.</creator><general>Elsevier Ireland Ltd</general><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>7TK</scope><scope>7X8</scope></search><sort><creationdate>19930319</creationdate><title>Modulation of IGF-2 expression during growth and differentiation of human neuroblastoma cells: Retinoic acid may induce IGF-2</title><author>Melino, Gerry ; Stephanou, Anastasis ; Annicchiarico-Petruzzelli, Margherita ; Knight, Richard A. ; Finazzi-Agro, Alessandro ; Lightman, Stafford L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c388t-71f14ac69000da3f1ec5df1431dbb3bade61c61f8a34ee7b7117ef52c00f50343</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Apoptosis</topic><topic>Brain Neoplasms - metabolism</topic><topic>Cell Differentiation - drug effects</topic><topic>Cell Movement - drug effects</topic><topic>Differentiation</topic><topic>GHRH</topic><topic>Growth Hormone - biosynthesis</topic><topic>Humans</topic><topic>IGF-2</topic><topic>Indicators and Reagents</topic><topic>Insulin-Like Growth Factor II - biosynthesis</topic><topic>Neurites - drug effects</topic><topic>Neuroblastoma</topic><topic>Neuroblastoma - metabolism</topic><topic>Programmed cell death</topic><topic>Retinoić acid</topic><topic>RNA, Messenger - biosynthesis</topic><topic>Tretinoin - pharmacology</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Melino, Gerry</creatorcontrib><creatorcontrib>Stephanou, Anastasis</creatorcontrib><creatorcontrib>Annicchiarico-Petruzzelli, Margherita</creatorcontrib><creatorcontrib>Knight, Richard A.</creatorcontrib><creatorcontrib>Finazzi-Agro, Alessandro</creatorcontrib><creatorcontrib>Lightman, Stafford L.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Neuroscience letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Melino, Gerry</au><au>Stephanou, Anastasis</au><au>Annicchiarico-Petruzzelli, Margherita</au><au>Knight, Richard A.</au><au>Finazzi-Agro, Alessandro</au><au>Lightman, Stafford L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Modulation of IGF-2 expression during growth and differentiation of human neuroblastoma cells: Retinoic acid may induce IGF-2</atitle><jtitle>Neuroscience letters</jtitle><addtitle>Neurosci Lett</addtitle><date>1993-03-19</date><risdate>1993</risdate><volume>151</volume><issue>2</issue><spage>187</spage><epage>191</epage><pages>187-191</pages><issn>0304-3940</issn><eissn>1872-7972</eissn><abstract>Insulin-like growth factor 2 (IGF-2) is the major autocrine growth factor for neuroblastoma. IGF-2 mRNA can just be detected in SK-N-BE(2) cell line; higher levels are present in two clones derived from it [BE(2)-C; BE(2)-M17]. IGF-2 mRNA is increased by retinoic acid (RA) only in the clones. IGF-2 expression/induction is more marked in BE(2)-M17, which shows more RA-resistance (evaluated as growth inhibition, neurite outgrowth and induction of programmed cell death). Under RA exposure, the parental line shows a more pronounced growth inhibition, neurite outgrowth and programmed cell death, as compared to its clones. BE(2)-C cells also express type 1 IGF receptor mRNA, though with a different time course than for expression of IGF-2. The data suggest that IGF-2 expression is correlated with growth, and may counteract the growth retardation, neurite outgrowth and programmed cell death effects of retinoic acid. Therefore the autocrine pattern of IGF-2 production by neuroblastoma cells may promote RA-resistance.</abstract><cop>Ireland</cop><pub>Elsevier Ireland Ltd</pub><pmid>8506078</pmid><doi>10.1016/0304-3940(93)90017-F</doi><tpages>5</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0304-3940 |
| ispartof | Neuroscience letters, 1993-03, Vol.151 (2), p.187-191 |
| issn | 0304-3940 1872-7972 |
| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Apoptosis Brain Neoplasms - metabolism Cell Differentiation - drug effects Cell Movement - drug effects Differentiation GHRH Growth Hormone - biosynthesis Humans IGF-2 Indicators and Reagents Insulin-Like Growth Factor II - biosynthesis Neurites - drug effects Neuroblastoma Neuroblastoma - metabolism Programmed cell death Retinoić acid RNA, Messenger - biosynthesis Tretinoin - pharmacology Tumor Cells, Cultured |
| title | Modulation of IGF-2 expression during growth and differentiation of human neuroblastoma cells: Retinoic acid may induce IGF-2 |
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