Insulin-like growth factor 1 (IGF-1) alters drug sensitivity of HBL100 human breast cancer cells by inhibition of apoptosis induced by diverse anticancer drugs
In this study, we tested the hypothesis that insulin-like growth factor-1 (IGF-1) modulates apoptosis in human breast cancer cells, HBL100, induced by diverse chemotherapeutic drugs. IGF-1 increased cell survival of HBL100 cells treated with 5-fluorouracil (antimetabolite), methotrexate (antimetabol...
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| Veröffentlicht in: | Cancer research (Chicago, Ill.) Ill.), 1997-07, Vol.57 (13), p.2687-2693 |
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| creator | DUNN, S. E HARDMAN, R. A KARI, F. W BARRETT, J. C |
| description | In this study, we tested the hypothesis that insulin-like growth factor-1 (IGF-1) modulates apoptosis in human breast cancer cells, HBL100, induced by diverse chemotherapeutic drugs. IGF-1 increased cell survival of HBL100 cells treated with 5-fluorouracil (antimetabolite), methotrexate (antimetabolite), tamoxifen (antiestrogen/antiproliferative), or camptothecin (topoisomerase 1 inhibitor) and after serum withdrawal. Elevated cell survival was not due to an increase in cell proliferation by IGF-1, but rather to an inhibition of apoptosis. Evidence for death by apoptosis was supported by cellular morphology and DNA fragmentation. There were no changes observed in Bcl-2 protein or bax mRNA levels. Extracellular matrix (ECM) is known to influence the apoptotic response of cells; therefore, the antiapoptotic effect of IGF-1 on breast cancer cells was examined using different ECMs: laminin, collagen IV, or Matrigel. IGF-1 protected cells from apoptosis induced by methotrexate on all ECMs tested, providing the first evidence that IGF-1 protects against apoptosis in three-dimensional culture systems. These data provide the rationale to search for drugs that lower serum IGF-1 in an effort to improve the efficacy of chemotherapeutic drugs for the treatment of breast cancer. |
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E ; HARDMAN, R. A ; KARI, F. W ; BARRETT, J. C</creator><creatorcontrib>DUNN, S. E ; HARDMAN, R. A ; KARI, F. W ; BARRETT, J. C</creatorcontrib><description>In this study, we tested the hypothesis that insulin-like growth factor-1 (IGF-1) modulates apoptosis in human breast cancer cells, HBL100, induced by diverse chemotherapeutic drugs. IGF-1 increased cell survival of HBL100 cells treated with 5-fluorouracil (antimetabolite), methotrexate (antimetabolite), tamoxifen (antiestrogen/antiproliferative), or camptothecin (topoisomerase 1 inhibitor) and after serum withdrawal. Elevated cell survival was not due to an increase in cell proliferation by IGF-1, but rather to an inhibition of apoptosis. Evidence for death by apoptosis was supported by cellular morphology and DNA fragmentation. There were no changes observed in Bcl-2 protein or bax mRNA levels. Extracellular matrix (ECM) is known to influence the apoptotic response of cells; therefore, the antiapoptotic effect of IGF-1 on breast cancer cells was examined using different ECMs: laminin, collagen IV, or Matrigel. IGF-1 protected cells from apoptosis induced by methotrexate on all ECMs tested, providing the first evidence that IGF-1 protects against apoptosis in three-dimensional culture systems. These data provide the rationale to search for drugs that lower serum IGF-1 in an effort to improve the efficacy of chemotherapeutic drugs for the treatment of breast cancer.</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>PMID: 9205078</identifier><identifier>CODEN: CNREA8</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Antineoplastic agents ; Antineoplastic Agents - pharmacology ; Apoptosis - drug effects ; bcl-2-Associated X Protein ; Biological and medical sciences ; Blotting, Northern ; Blotting, Western ; Breast Neoplasms - drug therapy ; Breast Neoplasms - ultrastructure ; Camptothecin - pharmacology ; Cell Survival - drug effects ; Collagen - physiology ; Drug Combinations ; Extracellular Matrix - physiology ; Female ; Fluorouracil - pharmacology ; General aspects ; Humans ; Insulin-Like Growth Factor I - pharmacology ; Laminin - physiology ; Medical sciences ; Methotrexate - pharmacology ; Microscopy, Electron ; Pharmacology. Drug treatments ; Proteoglycans - physiology ; Proto-Oncogene Proteins - metabolism ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; Tamoxifen - pharmacology ; Time Factors ; Tumor Cells, Cultured</subject><ispartof>Cancer research (Chicago, Ill.), 1997-07, Vol.57 (13), p.2687-2693</ispartof><rights>1997 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2790944$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9205078$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>DUNN, S. E</creatorcontrib><creatorcontrib>HARDMAN, R. A</creatorcontrib><creatorcontrib>KARI, F. W</creatorcontrib><creatorcontrib>BARRETT, J. C</creatorcontrib><title>Insulin-like growth factor 1 (IGF-1) alters drug sensitivity of HBL100 human breast cancer cells by inhibition of apoptosis induced by diverse anticancer drugs</title><title>Cancer research (Chicago, Ill.)</title><addtitle>Cancer Res</addtitle><description>In this study, we tested the hypothesis that insulin-like growth factor-1 (IGF-1) modulates apoptosis in human breast cancer cells, HBL100, induced by diverse chemotherapeutic drugs. IGF-1 increased cell survival of HBL100 cells treated with 5-fluorouracil (antimetabolite), methotrexate (antimetabolite), tamoxifen (antiestrogen/antiproliferative), or camptothecin (topoisomerase 1 inhibitor) and after serum withdrawal. Elevated cell survival was not due to an increase in cell proliferation by IGF-1, but rather to an inhibition of apoptosis. Evidence for death by apoptosis was supported by cellular morphology and DNA fragmentation. There were no changes observed in Bcl-2 protein or bax mRNA levels. Extracellular matrix (ECM) is known to influence the apoptotic response of cells; therefore, the antiapoptotic effect of IGF-1 on breast cancer cells was examined using different ECMs: laminin, collagen IV, or Matrigel. IGF-1 protected cells from apoptosis induced by methotrexate on all ECMs tested, providing the first evidence that IGF-1 protects against apoptosis in three-dimensional culture systems. These data provide the rationale to search for drugs that lower serum IGF-1 in an effort to improve the efficacy of chemotherapeutic drugs for the treatment of breast cancer.</description><subject>Antineoplastic agents</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Apoptosis - drug effects</subject><subject>bcl-2-Associated X Protein</subject><subject>Biological and medical sciences</subject><subject>Blotting, Northern</subject><subject>Blotting, Western</subject><subject>Breast Neoplasms - drug therapy</subject><subject>Breast Neoplasms - ultrastructure</subject><subject>Camptothecin - pharmacology</subject><subject>Cell Survival - drug effects</subject><subject>Collagen - physiology</subject><subject>Drug Combinations</subject><subject>Extracellular Matrix - physiology</subject><subject>Female</subject><subject>Fluorouracil - pharmacology</subject><subject>General aspects</subject><subject>Humans</subject><subject>Insulin-Like Growth Factor I - pharmacology</subject><subject>Laminin - physiology</subject><subject>Medical sciences</subject><subject>Methotrexate - pharmacology</subject><subject>Microscopy, Electron</subject><subject>Pharmacology. Drug treatments</subject><subject>Proteoglycans - physiology</subject><subject>Proto-Oncogene Proteins - metabolism</subject><subject>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject><subject>Tamoxifen - pharmacology</subject><subject>Time Factors</subject><subject>Tumor Cells, Cultured</subject><issn>0008-5472</issn><issn>1538-7445</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9UN1KwzAULqLM-fMIQi5E9KJwkiZteqnDucHAG70eaZJu0S6dOelkT-Or2mLx6nDO98d3TpIpFZlMC87FaTIFAJkKXrDz5ALxo18FBTFJJiUDAYWcJj9Lj13jfNq4T0s2of2OW1IrHdtAKLlfvsxT-kBUE21AYkK3IWg9uugOLh5JW5PF04oCkG23U55UwSqMRCuvbSDaNg2S6kic37qq17R-UKh9u48tOuzvptPWDBTjDn2CJcpHN8qHNLxKzmrVoL0e52XyPn9-my3S1evLcva4SrcZQEyrvPfJaqZKVunMmtzIHGRtQQItoFBCMgDGlTG6pAWTlZZQlFoDcM5zXmaXyd2f7z60X53FuN45HAoob9sO1zQHIRgdiDcjsat21qz3we1UOK7Hj_b47Ygr1KqpQ1_G4T-NFSWUnGe_k4aAkw</recordid><startdate>19970701</startdate><enddate>19970701</enddate><creator>DUNN, S. E</creator><creator>HARDMAN, R. A</creator><creator>KARI, F. W</creator><creator>BARRETT, J. C</creator><general>American Association for Cancer Research</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7TO</scope><scope>H94</scope></search><sort><creationdate>19970701</creationdate><title>Insulin-like growth factor 1 (IGF-1) alters drug sensitivity of HBL100 human breast cancer cells by inhibition of apoptosis induced by diverse anticancer drugs</title><author>DUNN, S. E ; HARDMAN, R. A ; KARI, F. W ; BARRETT, J. C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h300t-b6ced3f2a92bc3ed6d8608fe0801707a5820024addc91728bc8079cc004446493</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Antineoplastic agents</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Apoptosis - drug effects</topic><topic>bcl-2-Associated X Protein</topic><topic>Biological and medical sciences</topic><topic>Blotting, Northern</topic><topic>Blotting, Western</topic><topic>Breast Neoplasms - drug therapy</topic><topic>Breast Neoplasms - ultrastructure</topic><topic>Camptothecin - pharmacology</topic><topic>Cell Survival - drug effects</topic><topic>Collagen - physiology</topic><topic>Drug Combinations</topic><topic>Extracellular Matrix - physiology</topic><topic>Female</topic><topic>Fluorouracil - pharmacology</topic><topic>General aspects</topic><topic>Humans</topic><topic>Insulin-Like Growth Factor I - pharmacology</topic><topic>Laminin - physiology</topic><topic>Medical sciences</topic><topic>Methotrexate - pharmacology</topic><topic>Microscopy, Electron</topic><topic>Pharmacology. Drug treatments</topic><topic>Proteoglycans - physiology</topic><topic>Proto-Oncogene Proteins - metabolism</topic><topic>Proto-Oncogene Proteins c-bcl-2 - metabolism</topic><topic>Tamoxifen - pharmacology</topic><topic>Time Factors</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>DUNN, S. E</creatorcontrib><creatorcontrib>HARDMAN, R. A</creatorcontrib><creatorcontrib>KARI, F. W</creatorcontrib><creatorcontrib>BARRETT, J. 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C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Insulin-like growth factor 1 (IGF-1) alters drug sensitivity of HBL100 human breast cancer cells by inhibition of apoptosis induced by diverse anticancer drugs</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><addtitle>Cancer Res</addtitle><date>1997-07-01</date><risdate>1997</risdate><volume>57</volume><issue>13</issue><spage>2687</spage><epage>2693</epage><pages>2687-2693</pages><issn>0008-5472</issn><eissn>1538-7445</eissn><coden>CNREA8</coden><abstract>In this study, we tested the hypothesis that insulin-like growth factor-1 (IGF-1) modulates apoptosis in human breast cancer cells, HBL100, induced by diverse chemotherapeutic drugs. IGF-1 increased cell survival of HBL100 cells treated with 5-fluorouracil (antimetabolite), methotrexate (antimetabolite), tamoxifen (antiestrogen/antiproliferative), or camptothecin (topoisomerase 1 inhibitor) and after serum withdrawal. Elevated cell survival was not due to an increase in cell proliferation by IGF-1, but rather to an inhibition of apoptosis. Evidence for death by apoptosis was supported by cellular morphology and DNA fragmentation. There were no changes observed in Bcl-2 protein or bax mRNA levels. Extracellular matrix (ECM) is known to influence the apoptotic response of cells; therefore, the antiapoptotic effect of IGF-1 on breast cancer cells was examined using different ECMs: laminin, collagen IV, or Matrigel. IGF-1 protected cells from apoptosis induced by methotrexate on all ECMs tested, providing the first evidence that IGF-1 protects against apoptosis in three-dimensional culture systems. These data provide the rationale to search for drugs that lower serum IGF-1 in an effort to improve the efficacy of chemotherapeutic drugs for the treatment of breast cancer.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>9205078</pmid><tpages>7</tpages></addata></record> |
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| source | MEDLINE; American Association for Cancer Research; EZB-FREE-00999 freely available EZB journals |
| subjects | Antineoplastic agents Antineoplastic Agents - pharmacology Apoptosis - drug effects bcl-2-Associated X Protein Biological and medical sciences Blotting, Northern Blotting, Western Breast Neoplasms - drug therapy Breast Neoplasms - ultrastructure Camptothecin - pharmacology Cell Survival - drug effects Collagen - physiology Drug Combinations Extracellular Matrix - physiology Female Fluorouracil - pharmacology General aspects Humans Insulin-Like Growth Factor I - pharmacology Laminin - physiology Medical sciences Methotrexate - pharmacology Microscopy, Electron Pharmacology. Drug treatments Proteoglycans - physiology Proto-Oncogene Proteins - metabolism Proto-Oncogene Proteins c-bcl-2 - metabolism Tamoxifen - pharmacology Time Factors Tumor Cells, Cultured |
| title | Insulin-like growth factor 1 (IGF-1) alters drug sensitivity of HBL100 human breast cancer cells by inhibition of apoptosis induced by diverse anticancer drugs |
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