Effects of Anandamide on Polyamine Levels and Cell Growth in Human Colon Cancer Cells
Anandamide (AEA) is an endogenous agonist for cannabinoid receptor CB1-R and seems to be involved in the control of cancer growth. Polyamines are compounds that play an important role in cell proliferation and differentiation. Our aim was to investigate the effect of AEA on the polyamine levels (put...
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Veröffentlicht in: | Anticancer research 2010-07, Vol.30 (7), p.2583-2589 |
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creator | LINSALATA, Michele NOTARNICOLA, Maria TUTINO, Valeria BIFULCO, Maurizio SANTORO, Antonietta LAEZZA, Chiara MESSA, Caterina ORLANDO, Antonella GABRIELLA CARUSO, Maria |
description | Anandamide (AEA) is an endogenous agonist for cannabinoid receptor CB1-R and seems to be involved in the control of cancer growth. Polyamines are compounds that play an important role in cell proliferation and differentiation. Our aim was to investigate the effect of AEA on the polyamine levels (putrescine, spermidine and spermine) and cell growth of three human colon cancer cell lines, positive for CB1-R.
After AEA treatment of DLD-1, HT-29 and SW620 cells, polyamine analysis was performed by high-performance liquid chromatography (HPLC) and cell growth was measured by 3-(4,5 di-methylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) test. CB1 gene expression was determined using reverse transcription and polymerase chain reaction (RT-PCR).
AEA significantly reduced polyamine levels and cell proliferation dose-dependently when the tested cell lines were exposed for 24 h and 48 h. This inhibitory effect was mediated by CB1-R, since SR 1411716A, a selective CB-1 receptor antagonist, was able to entirely antagonize the effect of AEA. CB1-R mRNA levels were enhanced after AEA treatment in DLD-1 cells, whereas no induction was found in HT-29 and SW620 cells.
It appears that mechanisms by which AEA may affect growth of colon cancer cells involve a decrease in cell proliferation rate by reducing the polyamine levels. |
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After AEA treatment of DLD-1, HT-29 and SW620 cells, polyamine analysis was performed by high-performance liquid chromatography (HPLC) and cell growth was measured by 3-(4,5 di-methylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) test. CB1 gene expression was determined using reverse transcription and polymerase chain reaction (RT-PCR).
AEA significantly reduced polyamine levels and cell proliferation dose-dependently when the tested cell lines were exposed for 24 h and 48 h. This inhibitory effect was mediated by CB1-R, since SR 1411716A, a selective CB-1 receptor antagonist, was able to entirely antagonize the effect of AEA. CB1-R mRNA levels were enhanced after AEA treatment in DLD-1 cells, whereas no induction was found in HT-29 and SW620 cells.
It appears that mechanisms by which AEA may affect growth of colon cancer cells involve a decrease in cell proliferation rate by reducing the polyamine levels.</description><identifier>ISSN: 0250-7005</identifier><identifier>EISSN: 1791-7530</identifier><identifier>PMID: 20682986</identifier><language>eng</language><publisher>Attiki: International Institute of Anticancer Research</publisher><subject>Arachidonic Acids - pharmacology ; Biogenic Polyamines - metabolism ; Biological and medical sciences ; Cell Differentiation - physiology ; Cell Growth Processes - drug effects ; Colonic Neoplasms - drug therapy ; Colonic Neoplasms - metabolism ; Colonic Neoplasms - pathology ; Dose-Response Relationship, Drug ; Endocannabinoids ; Gastroenterology. Liver. Pancreas. Abdomen ; Gene Expression - drug effects ; HT29 Cells ; Humans ; Medical sciences ; Polyunsaturated Alkamides - pharmacology ; Receptor, Cannabinoid, CB1 - agonists ; Receptor, Cannabinoid, CB1 - biosynthesis ; Receptor, Cannabinoid, CB1 - genetics ; Receptor, Cannabinoid, CB1 - metabolism ; RNA, Messenger - biosynthesis ; RNA, Messenger - genetics ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Tumors</subject><ispartof>Anticancer research, 2010-07, Vol.30 (7), p.2583-2589</ispartof><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23078969$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20682986$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>LINSALATA, Michele</creatorcontrib><creatorcontrib>NOTARNICOLA, Maria</creatorcontrib><creatorcontrib>TUTINO, Valeria</creatorcontrib><creatorcontrib>BIFULCO, Maurizio</creatorcontrib><creatorcontrib>SANTORO, Antonietta</creatorcontrib><creatorcontrib>LAEZZA, Chiara</creatorcontrib><creatorcontrib>MESSA, Caterina</creatorcontrib><creatorcontrib>ORLANDO, Antonella</creatorcontrib><creatorcontrib>GABRIELLA CARUSO, Maria</creatorcontrib><title>Effects of Anandamide on Polyamine Levels and Cell Growth in Human Colon Cancer Cells</title><title>Anticancer research</title><addtitle>Anticancer Res</addtitle><description>Anandamide (AEA) is an endogenous agonist for cannabinoid receptor CB1-R and seems to be involved in the control of cancer growth. Polyamines are compounds that play an important role in cell proliferation and differentiation. Our aim was to investigate the effect of AEA on the polyamine levels (putrescine, spermidine and spermine) and cell growth of three human colon cancer cell lines, positive for CB1-R.
After AEA treatment of DLD-1, HT-29 and SW620 cells, polyamine analysis was performed by high-performance liquid chromatography (HPLC) and cell growth was measured by 3-(4,5 di-methylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) test. CB1 gene expression was determined using reverse transcription and polymerase chain reaction (RT-PCR).
AEA significantly reduced polyamine levels and cell proliferation dose-dependently when the tested cell lines were exposed for 24 h and 48 h. This inhibitory effect was mediated by CB1-R, since SR 1411716A, a selective CB-1 receptor antagonist, was able to entirely antagonize the effect of AEA. CB1-R mRNA levels were enhanced after AEA treatment in DLD-1 cells, whereas no induction was found in HT-29 and SW620 cells.
It appears that mechanisms by which AEA may affect growth of colon cancer cells involve a decrease in cell proliferation rate by reducing the polyamine levels.</description><subject>Arachidonic Acids - pharmacology</subject><subject>Biogenic Polyamines - metabolism</subject><subject>Biological and medical sciences</subject><subject>Cell Differentiation - physiology</subject><subject>Cell Growth Processes - drug effects</subject><subject>Colonic Neoplasms - drug therapy</subject><subject>Colonic Neoplasms - metabolism</subject><subject>Colonic Neoplasms - pathology</subject><subject>Dose-Response Relationship, Drug</subject><subject>Endocannabinoids</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Gene Expression - drug effects</subject><subject>HT29 Cells</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Polyunsaturated Alkamides - pharmacology</subject><subject>Receptor, Cannabinoid, CB1 - agonists</subject><subject>Receptor, Cannabinoid, CB1 - biosynthesis</subject><subject>Receptor, Cannabinoid, CB1 - genetics</subject><subject>Receptor, Cannabinoid, CB1 - metabolism</subject><subject>RNA, Messenger - biosynthesis</subject><subject>RNA, Messenger - genetics</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>Tumors</subject><issn>0250-7005</issn><issn>1791-7530</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpF0F9LwzAQAPAgipvTryB5EZ8KaZLmz-Mo0wkDfXDP5ZomWEmT2bTKvr1BJz4dd_fjuLsztCylLgtZMXKOloRWpJCEVAt0ldI7IUJoxS7RghKhqFZiifYb56yZEo4OrwOEDoa-szgG_BL9MSfB4p39tD7h3MS19R4_jvFresN9wNt5gIDr6LOvIRg7_oh0jS4c-GRvTnGF9g-b13pb7J4fn-r1rjhQTqaC0865jlayJdxIZ9rSVI4w2oK0ipQgtNUWpBYtFQY6oXhZAQOnDXU0F9kK3f_OPYzxY7ZpaoY-mbwBBBvn1EiuNOeSkSxvT3JuB9s1h7EfYDw2f5_I4O4EIBnwbszn9OnfMSKVFpp9A62kZ3A</recordid><startdate>20100701</startdate><enddate>20100701</enddate><creator>LINSALATA, Michele</creator><creator>NOTARNICOLA, Maria</creator><creator>TUTINO, Valeria</creator><creator>BIFULCO, Maurizio</creator><creator>SANTORO, Antonietta</creator><creator>LAEZZA, Chiara</creator><creator>MESSA, Caterina</creator><creator>ORLANDO, Antonella</creator><creator>GABRIELLA CARUSO, Maria</creator><general>International Institute of Anticancer Research</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>20100701</creationdate><title>Effects of Anandamide on Polyamine Levels and Cell Growth in Human Colon Cancer Cells</title><author>LINSALATA, Michele ; NOTARNICOLA, Maria ; TUTINO, Valeria ; BIFULCO, Maurizio ; SANTORO, Antonietta ; LAEZZA, Chiara ; MESSA, Caterina ; ORLANDO, Antonella ; GABRIELLA CARUSO, Maria</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p240t-42dffd257b04c7fcb1c5f032ba7e801a69e9ea796b26cad68415a3af9c2f26b23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Arachidonic Acids - pharmacology</topic><topic>Biogenic Polyamines - metabolism</topic><topic>Biological and medical sciences</topic><topic>Cell Differentiation - physiology</topic><topic>Cell Growth Processes - drug effects</topic><topic>Colonic Neoplasms - drug therapy</topic><topic>Colonic Neoplasms - metabolism</topic><topic>Colonic Neoplasms - pathology</topic><topic>Dose-Response Relationship, Drug</topic><topic>Endocannabinoids</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Gene Expression - drug effects</topic><topic>HT29 Cells</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Polyunsaturated Alkamides - pharmacology</topic><topic>Receptor, Cannabinoid, CB1 - agonists</topic><topic>Receptor, Cannabinoid, CB1 - biosynthesis</topic><topic>Receptor, Cannabinoid, CB1 - genetics</topic><topic>Receptor, Cannabinoid, CB1 - metabolism</topic><topic>RNA, Messenger - biosynthesis</topic><topic>RNA, Messenger - genetics</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>LINSALATA, Michele</creatorcontrib><creatorcontrib>NOTARNICOLA, Maria</creatorcontrib><creatorcontrib>TUTINO, Valeria</creatorcontrib><creatorcontrib>BIFULCO, Maurizio</creatorcontrib><creatorcontrib>SANTORO, Antonietta</creatorcontrib><creatorcontrib>LAEZZA, Chiara</creatorcontrib><creatorcontrib>MESSA, Caterina</creatorcontrib><creatorcontrib>ORLANDO, Antonella</creatorcontrib><creatorcontrib>GABRIELLA CARUSO, Maria</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>MEDLINE - Academic</collection><jtitle>Anticancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>LINSALATA, Michele</au><au>NOTARNICOLA, Maria</au><au>TUTINO, Valeria</au><au>BIFULCO, Maurizio</au><au>SANTORO, Antonietta</au><au>LAEZZA, Chiara</au><au>MESSA, Caterina</au><au>ORLANDO, Antonella</au><au>GABRIELLA CARUSO, Maria</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of Anandamide on Polyamine Levels and Cell Growth in Human Colon Cancer Cells</atitle><jtitle>Anticancer research</jtitle><addtitle>Anticancer Res</addtitle><date>2010-07-01</date><risdate>2010</risdate><volume>30</volume><issue>7</issue><spage>2583</spage><epage>2589</epage><pages>2583-2589</pages><issn>0250-7005</issn><eissn>1791-7530</eissn><abstract>Anandamide (AEA) is an endogenous agonist for cannabinoid receptor CB1-R and seems to be involved in the control of cancer growth. Polyamines are compounds that play an important role in cell proliferation and differentiation. Our aim was to investigate the effect of AEA on the polyamine levels (putrescine, spermidine and spermine) and cell growth of three human colon cancer cell lines, positive for CB1-R.
After AEA treatment of DLD-1, HT-29 and SW620 cells, polyamine analysis was performed by high-performance liquid chromatography (HPLC) and cell growth was measured by 3-(4,5 di-methylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) test. CB1 gene expression was determined using reverse transcription and polymerase chain reaction (RT-PCR).
AEA significantly reduced polyamine levels and cell proliferation dose-dependently when the tested cell lines were exposed for 24 h and 48 h. This inhibitory effect was mediated by CB1-R, since SR 1411716A, a selective CB-1 receptor antagonist, was able to entirely antagonize the effect of AEA. CB1-R mRNA levels were enhanced after AEA treatment in DLD-1 cells, whereas no induction was found in HT-29 and SW620 cells.
It appears that mechanisms by which AEA may affect growth of colon cancer cells involve a decrease in cell proliferation rate by reducing the polyamine levels.</abstract><cop>Attiki</cop><pub>International Institute of Anticancer Research</pub><pmid>20682986</pmid><tpages>7</tpages></addata></record> |
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subjects | Arachidonic Acids - pharmacology Biogenic Polyamines - metabolism Biological and medical sciences Cell Differentiation - physiology Cell Growth Processes - drug effects Colonic Neoplasms - drug therapy Colonic Neoplasms - metabolism Colonic Neoplasms - pathology Dose-Response Relationship, Drug Endocannabinoids Gastroenterology. Liver. Pancreas. Abdomen Gene Expression - drug effects HT29 Cells Humans Medical sciences Polyunsaturated Alkamides - pharmacology Receptor, Cannabinoid, CB1 - agonists Receptor, Cannabinoid, CB1 - biosynthesis Receptor, Cannabinoid, CB1 - genetics Receptor, Cannabinoid, CB1 - metabolism RNA, Messenger - biosynthesis RNA, Messenger - genetics Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Tumors |
title | Effects of Anandamide on Polyamine Levels and Cell Growth in Human Colon Cancer Cells |
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