Activation of insulin‐like growth factor I receptor‐mediated pathway by ginsenoside Rg1

Ginsenoside Rg1, an active ingredient in ginseng, was previously shown to be a novel class of potent phytoestrogen. The present study aims at investigating the molecular mechanisms involved in mediating its actions in human breast cancer (MCF‐7) cells. Rg1 (1 pM) stimulates cell proliferation (P

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Published in:British journal of pharmacology 2006-03, Vol.147 (5), p.542-551
Main Authors: Chen, Wen‐Fang, Lau, Wai‐Sum, Cheung, Pik‐Yuen, Guo, De‐An, Wong, Man‐Sau
Format: Article
Language:English
Subjects:
Biological and medical sciences
Cell Line
Cell Proliferation - drug effects
estrogen
Estrogen Receptor alpha - physiology
Ginsenoside Rg1
Ginsenosides - pharmacology
Gynecology. Andrology. Obstetrics
human breast cancer
Humans
Insulin-Like Growth Factor I - pharmacology
insulin‐like growth factor I receptor
Mammary gland diseases
Medical sciences
Pharmacology. Drug treatments
phytoestrogen
Promoter Regions, Genetic
Receptor, IGF Type 1 - drug effects
Receptor, IGF Type 1 - genetics
Receptor, IGF Type 1 - physiology
RNA, Messenger - analysis
Signal Transduction - drug effects
Trefoil Factor-1
Tumor Suppressor Proteins - genetics
Tumors
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creator Chen, Wen‐Fang
Lau, Wai‐Sum
Cheung, Pik‐Yuen
Guo, De‐An
Wong, Man‐Sau
description Ginsenoside Rg1, an active ingredient in ginseng, was previously shown to be a novel class of potent phytoestrogen. The present study aims at investigating the molecular mechanisms involved in mediating its actions in human breast cancer (MCF‐7) cells. Rg1 (1 pM) stimulates cell proliferation (P
doi_str_mv 10.1038/sj.bjp.0706640
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The present study aims at investigating the molecular mechanisms involved in mediating its actions in human breast cancer (MCF‐7) cells. Rg1 (1 pM) stimulates cell proliferation (P&lt;0.01) and estrogen‐responsive pS2 mRNA expression (P&lt;0.05) without alteration of estrogen receptor alpha (ERα) protein or mRNA expression in MCF‐7 cells. In addition, 10−14–10−4 M of Rg1 does not demonstrate specific binding to ERα. We hypothesize that Rg1 may exert its actions in MCF‐7 cell via the activation of crosstalk between ER‐ and insulin growth factor I receptor (IGF‐IR)‐dependent pathways. The results indicate that Rg1 significantly increases IGF‐IR expression and IGF‐IR promoter activity in MCF‐7 cells (P&lt;0.05). Cotreatment of MCF‐7 cells with 1 μM of estrogen antagonist ICI 182,780 completely abolishes the effects of Rg1 on IGF‐IR expression. Furthermore, Rg1 enhances tyrosine phosphorylation of IRS‐1 in MCF‐7 cells upon IGF‐I stimulation and the activation of IRS‐1 phosphorylation is also ER‐dependent. Taken together, our results suggest that Rg1 not only increases IGF‐IR expression but also enhances IGF‐IR‐mediated signaling pathways in MCF‐7 cells. The stimulation of IGF‐IR expression by Rg1 in MCF‐7 cells appears to require ER, and its actions might involve ligand‐independent activation of ER. British Journal of Pharmacology (2006) 147, 542–551. doi:10.1038/sj.bjp.0706640</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1038/sj.bjp.0706640</identifier><identifier>PMID: 16415910</identifier><identifier>CODEN: BJPCBM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Biological and medical sciences ; Cell Line ; Cell Proliferation - drug effects ; estrogen ; Estrogen Receptor alpha - physiology ; Ginsenoside Rg1 ; Ginsenosides - pharmacology ; Gynecology. Andrology. Obstetrics ; human breast cancer ; Humans ; Insulin-Like Growth Factor I - pharmacology ; insulin‐like growth factor I receptor ; Mammary gland diseases ; Medical sciences ; Pharmacology. Drug treatments ; phytoestrogen ; Promoter Regions, Genetic ; Receptor, IGF Type 1 - drug effects ; Receptor, IGF Type 1 - genetics ; Receptor, IGF Type 1 - physiology ; RNA, Messenger - analysis ; Signal Transduction - drug effects ; Trefoil Factor-1 ; Tumor Suppressor Proteins - genetics ; Tumors</subject><ispartof>British journal of pharmacology, 2006-03, Vol.147 (5), p.542-551</ispartof><rights>2006 British Pharmacological Society</rights><rights>2006 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Mar 2006</rights><rights>Copyright 2006, Nature Publishing Group 2006 Nature Publishing Group</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5551-15f598e63523c06aec9213eae0dda41131f0711d8f3ed977994780389ad49a83</citedby><cites>FETCH-LOGICAL-c5551-15f598e63523c06aec9213eae0dda41131f0711d8f3ed977994780389ad49a83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1616975/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1616975/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=17710129$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16415910$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Wen‐Fang</creatorcontrib><creatorcontrib>Lau, Wai‐Sum</creatorcontrib><creatorcontrib>Cheung, Pik‐Yuen</creatorcontrib><creatorcontrib>Guo, De‐An</creatorcontrib><creatorcontrib>Wong, Man‐Sau</creatorcontrib><title>Activation of insulin‐like growth factor I receptor‐mediated pathway by ginsenoside Rg1</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>Ginsenoside Rg1, an active ingredient in ginseng, was previously shown to be a novel class of potent phytoestrogen. The present study aims at investigating the molecular mechanisms involved in mediating its actions in human breast cancer (MCF‐7) cells. Rg1 (1 pM) stimulates cell proliferation (P&lt;0.01) and estrogen‐responsive pS2 mRNA expression (P&lt;0.05) without alteration of estrogen receptor alpha (ERα) protein or mRNA expression in MCF‐7 cells. In addition, 10−14–10−4 M of Rg1 does not demonstrate specific binding to ERα. We hypothesize that Rg1 may exert its actions in MCF‐7 cell via the activation of crosstalk between ER‐ and insulin growth factor I receptor (IGF‐IR)‐dependent pathways. The results indicate that Rg1 significantly increases IGF‐IR expression and IGF‐IR promoter activity in MCF‐7 cells (P&lt;0.05). Cotreatment of MCF‐7 cells with 1 μM of estrogen antagonist ICI 182,780 completely abolishes the effects of Rg1 on IGF‐IR expression. Furthermore, Rg1 enhances tyrosine phosphorylation of IRS‐1 in MCF‐7 cells upon IGF‐I stimulation and the activation of IRS‐1 phosphorylation is also ER‐dependent. Taken together, our results suggest that Rg1 not only increases IGF‐IR expression but also enhances IGF‐IR‐mediated signaling pathways in MCF‐7 cells. The stimulation of IGF‐IR expression by Rg1 in MCF‐7 cells appears to require ER, and its actions might involve ligand‐independent activation of ER. British Journal of Pharmacology (2006) 147, 542–551. doi:10.1038/sj.bjp.0706640</description><subject>Biological and medical sciences</subject><subject>Cell Line</subject><subject>Cell Proliferation - drug effects</subject><subject>estrogen</subject><subject>Estrogen Receptor alpha - physiology</subject><subject>Ginsenoside Rg1</subject><subject>Ginsenosides - pharmacology</subject><subject>Gynecology. Andrology. 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The present study aims at investigating the molecular mechanisms involved in mediating its actions in human breast cancer (MCF‐7) cells. Rg1 (1 pM) stimulates cell proliferation (P&lt;0.01) and estrogen‐responsive pS2 mRNA expression (P&lt;0.05) without alteration of estrogen receptor alpha (ERα) protein or mRNA expression in MCF‐7 cells. In addition, 10−14–10−4 M of Rg1 does not demonstrate specific binding to ERα. We hypothesize that Rg1 may exert its actions in MCF‐7 cell via the activation of crosstalk between ER‐ and insulin growth factor I receptor (IGF‐IR)‐dependent pathways. The results indicate that Rg1 significantly increases IGF‐IR expression and IGF‐IR promoter activity in MCF‐7 cells (P&lt;0.05). Cotreatment of MCF‐7 cells with 1 μM of estrogen antagonist ICI 182,780 completely abolishes the effects of Rg1 on IGF‐IR expression. Furthermore, Rg1 enhances tyrosine phosphorylation of IRS‐1 in MCF‐7 cells upon IGF‐I stimulation and the activation of IRS‐1 phosphorylation is also ER‐dependent. Taken together, our results suggest that Rg1 not only increases IGF‐IR expression but also enhances IGF‐IR‐mediated signaling pathways in MCF‐7 cells. The stimulation of IGF‐IR expression by Rg1 in MCF‐7 cells appears to require ER, and its actions might involve ligand‐independent activation of ER. British Journal of Pharmacology (2006) 147, 542–551. doi:10.1038/sj.bjp.0706640</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>16415910</pmid><doi>10.1038/sj.bjp.0706640</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record>
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subjects Biological and medical sciences
Cell Line
Cell Proliferation - drug effects
estrogen
Estrogen Receptor alpha - physiology
Ginsenoside Rg1
Ginsenosides - pharmacology
Gynecology. Andrology. Obstetrics
human breast cancer
Humans
Insulin-Like Growth Factor I - pharmacology
insulin‐like growth factor I receptor
Mammary gland diseases
Medical sciences
Pharmacology. Drug treatments
phytoestrogen
Promoter Regions, Genetic
Receptor, IGF Type 1 - drug effects
Receptor, IGF Type 1 - genetics
Receptor, IGF Type 1 - physiology
RNA, Messenger - analysis
Signal Transduction - drug effects
Trefoil Factor-1
Tumor Suppressor Proteins - genetics
Tumors
title Activation of insulin‐like growth factor I receptor‐mediated pathway by ginsenoside Rg1
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