The non-competitive metabotropic glutamate receptor-1 antagonist CPCCOEt inhibits the in vitro growth of human melanoma
Five decades ago, the dicarboxylic amino acid glutamate became recognized as the major excitatory neurotransmitter in the central nervous system. In recent years, the expression of glutamate receptors was detected also in peripheral, non-neuronal tissues. Furthermore, it was found that glutamate sti...
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Veröffentlicht in: | Oncology reports 2007-06, Vol.17 (6), p.1399-1404 |
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description | Five decades ago, the dicarboxylic amino acid glutamate became recognized as the major excitatory neurotransmitter in the central nervous system. In recent years, the expression of glutamate receptors was detected also in peripheral, non-neuronal tissues. Furthermore, it was found that glutamate stimulated the proliferation and migration of several peripheral tumor cells, and that glutamate receptor antagonists limited tumor growth. Most of these studies, however, used broad spectrum compounds and/or group-specific antagonists. Here we report that a selective, non-competitive metabotropic glutamate receptor-1 antagonist, CPCCOEt (7-hydroxyiminocyclopropan[b]chromen-1a-carboxylic acid ethyl ester), significantly inhibited the proliferation and modified the morphology of two human melanoma cell lines. These effects were independent of the external glutamate level in the culture medium. In addition, CPCCOEt significantly enhanced the tumoricidal effects of cytostatic drugs. Thus, selective non-competitive metabotropic glutamate receptor antagonists may be used alone and/or with the synergistic effects of chemotherapy, thus enhancing existing therapies of melanoma and possibly other malignancies. |
doi_str_mv | 10.3892/or.17.6.1399 |
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In recent years, the expression of glutamate receptors was detected also in peripheral, non-neuronal tissues. Furthermore, it was found that glutamate stimulated the proliferation and migration of several peripheral tumor cells, and that glutamate receptor antagonists limited tumor growth. Most of these studies, however, used broad spectrum compounds and/or group-specific antagonists. Here we report that a selective, non-competitive metabotropic glutamate receptor-1 antagonist, CPCCOEt (7-hydroxyiminocyclopropan[b]chromen-1a-carboxylic acid ethyl ester), significantly inhibited the proliferation and modified the morphology of two human melanoma cell lines. These effects were independent of the external glutamate level in the culture medium. In addition, CPCCOEt significantly enhanced the tumoricidal effects of cytostatic drugs. Thus, selective non-competitive metabotropic glutamate receptor antagonists may be used alone and/or with the synergistic effects of chemotherapy, thus enhancing existing therapies of melanoma and possibly other malignancies.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.17.6.1399</identifier><identifier>PMID: 17487397</identifier><language>eng</language><publisher>Athens: S.n.</publisher><subject>Antineoplastic Agents - pharmacology ; Biological and medical sciences ; Cell Proliferation - drug effects ; Chromones - pharmacology ; Dermatology ; Drug Resistance, Neoplasm - drug effects ; Excitatory Amino Acid Antagonists - pharmacology ; Glutamic Acid - metabolism ; Humans ; Medical sciences ; Melanoma - metabolism ; Melanoma - ultrastructure ; Receptors, Metabotropic Glutamate - antagonists & inhibitors ; Skin Neoplasms - metabolism ; Skin Neoplasms - ultrastructure ; Taxoids - pharmacology ; Tumor Cells, Cultured ; Tumors ; Tumors of the skin and soft tissue. Premalignant lesions</subject><ispartof>Oncology reports, 2007-06, Vol.17 (6), p.1399-1404</ispartof><rights>2007 INIST-CNRS</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18782616$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17487397$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>HAAS, Helga Susanne</creatorcontrib><creatorcontrib>PFRAGNER, Roswitha</creatorcontrib><creatorcontrib>SIEGL, Veronika</creatorcontrib><creatorcontrib>INGOLIC, Elisabeth</creatorcontrib><creatorcontrib>HEINTZ, Elfgard</creatorcontrib><creatorcontrib>SCHRAML, Elisabeth</creatorcontrib><creatorcontrib>SCHAUENSTEIN, Konrad</creatorcontrib><title>The non-competitive metabotropic glutamate receptor-1 antagonist CPCCOEt inhibits the in vitro growth of human melanoma</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>Five decades ago, the dicarboxylic amino acid glutamate became recognized as the major excitatory neurotransmitter in the central nervous system. In recent years, the expression of glutamate receptors was detected also in peripheral, non-neuronal tissues. Furthermore, it was found that glutamate stimulated the proliferation and migration of several peripheral tumor cells, and that glutamate receptor antagonists limited tumor growth. Most of these studies, however, used broad spectrum compounds and/or group-specific antagonists. Here we report that a selective, non-competitive metabotropic glutamate receptor-1 antagonist, CPCCOEt (7-hydroxyiminocyclopropan[b]chromen-1a-carboxylic acid ethyl ester), significantly inhibited the proliferation and modified the morphology of two human melanoma cell lines. These effects were independent of the external glutamate level in the culture medium. In addition, CPCCOEt significantly enhanced the tumoricidal effects of cytostatic drugs. Thus, selective non-competitive metabotropic glutamate receptor antagonists may be used alone and/or with the synergistic effects of chemotherapy, thus enhancing existing therapies of melanoma and possibly other malignancies.</description><subject>Antineoplastic Agents - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Cell Proliferation - drug effects</subject><subject>Chromones - pharmacology</subject><subject>Dermatology</subject><subject>Drug Resistance, Neoplasm - drug effects</subject><subject>Excitatory Amino Acid Antagonists - pharmacology</subject><subject>Glutamic Acid - metabolism</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Melanoma - metabolism</subject><subject>Melanoma - ultrastructure</subject><subject>Receptors, Metabotropic Glutamate - antagonists & inhibitors</subject><subject>Skin Neoplasms - metabolism</subject><subject>Skin Neoplasms - ultrastructure</subject><subject>Taxoids - pharmacology</subject><subject>Tumor Cells, Cultured</subject><subject>Tumors</subject><subject>Tumors of the skin and soft tissue. 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Premalignant lesions</topic><toplevel>online_resources</toplevel><creatorcontrib>HAAS, Helga Susanne</creatorcontrib><creatorcontrib>PFRAGNER, Roswitha</creatorcontrib><creatorcontrib>SIEGL, Veronika</creatorcontrib><creatorcontrib>INGOLIC, Elisabeth</creatorcontrib><creatorcontrib>HEINTZ, Elfgard</creatorcontrib><creatorcontrib>SCHRAML, Elisabeth</creatorcontrib><creatorcontrib>SCHAUENSTEIN, Konrad</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>Oncology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>HAAS, Helga Susanne</au><au>PFRAGNER, Roswitha</au><au>SIEGL, Veronika</au><au>INGOLIC, Elisabeth</au><au>HEINTZ, Elfgard</au><au>SCHRAML, Elisabeth</au><au>SCHAUENSTEIN, Konrad</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The non-competitive metabotropic glutamate receptor-1 antagonist CPCCOEt inhibits the in vitro growth of human melanoma</atitle><jtitle>Oncology reports</jtitle><addtitle>Oncol Rep</addtitle><date>2007-06-01</date><risdate>2007</risdate><volume>17</volume><issue>6</issue><spage>1399</spage><epage>1404</epage><pages>1399-1404</pages><issn>1021-335X</issn><eissn>1791-2431</eissn><abstract>Five decades ago, the dicarboxylic amino acid glutamate became recognized as the major excitatory neurotransmitter in the central nervous system. In recent years, the expression of glutamate receptors was detected also in peripheral, non-neuronal tissues. Furthermore, it was found that glutamate stimulated the proliferation and migration of several peripheral tumor cells, and that glutamate receptor antagonists limited tumor growth. Most of these studies, however, used broad spectrum compounds and/or group-specific antagonists. Here we report that a selective, non-competitive metabotropic glutamate receptor-1 antagonist, CPCCOEt (7-hydroxyiminocyclopropan[b]chromen-1a-carboxylic acid ethyl ester), significantly inhibited the proliferation and modified the morphology of two human melanoma cell lines. These effects were independent of the external glutamate level in the culture medium. In addition, CPCCOEt significantly enhanced the tumoricidal effects of cytostatic drugs. 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subjects | Antineoplastic Agents - pharmacology Biological and medical sciences Cell Proliferation - drug effects Chromones - pharmacology Dermatology Drug Resistance, Neoplasm - drug effects Excitatory Amino Acid Antagonists - pharmacology Glutamic Acid - metabolism Humans Medical sciences Melanoma - metabolism Melanoma - ultrastructure Receptors, Metabotropic Glutamate - antagonists & inhibitors Skin Neoplasms - metabolism Skin Neoplasms - ultrastructure Taxoids - pharmacology Tumor Cells, Cultured Tumors Tumors of the skin and soft tissue. Premalignant lesions |
title | The non-competitive metabotropic glutamate receptor-1 antagonist CPCCOEt inhibits the in vitro growth of human melanoma |
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