Anti-androgen flutamide suppresses hepatocellular carcinoma cell proliferation via the aryl hydrocarbon receptor mediated induction of transforming growth factor-β1
The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor and a member of the basic helix-loop-helix PER/ARNT/SIM family of chemosensors and developmental regulators. The AhR is widely known as a mediator of dioxin toxicity; however, it also suppresses cancer cell proliferation...
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| Veröffentlicht in: | Oncogene 2015-12, Vol.34 (50), p.6092-6104 |
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| creator | Koch, D C Jang, H S O'Donnell, E F Punj, S Kopparapu, P R Bisson, W H Kerkvliet, N I Kolluri, S K |
| description | The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor and a member of the basic helix-loop-helix PER/ARNT/SIM family of chemosensors and developmental regulators. The AhR is widely known as a mediator of dioxin toxicity; however, it also suppresses cancer cell proliferation and recent findings have implicated its role as a tumor suppressor. We conducted a chemical library screen to identify nontoxic AhR ligands with anti-cancer effects and discovered flutamide (Eulexin) as a putative AhR ligand. Flutamide is an androgen receptor (AR) antagonist approved by the United States Food and Drug Administration for the treatment of prostate cancer. We found that flutamide inhibited the growth of several cancer cell lines independent of AR status, and that suppression of AhR expression reversed the anti-proliferative effects of flutamide. We investigated the AhR-dependent mechanism of action of flutamide in human hepatocellular carcinoma cells and identified that transforming growth factor-β1 (TGF-β1) is induced by flutamide in an AhR-dependent manner. In contrast, the potent AhR agonist 2,3,7,8-Tetrachlorodibenzo-p-dioxin had no effect on TGF-β1 expression, indicating the ligand specificity of AhR activation. We also determined that TGF-β1 induction is required for the AhR-dependent growth inhibitory effects of flutamide. Therefore, flutamide may be effective in AhR-positive cancers that are sensitive to TGF-β1 signaling, such as hepatocellular carcinoma. |
| doi_str_mv | 10.1038/onc.2015.55 |
| format | Article |
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The AhR is widely known as a mediator of dioxin toxicity; however, it also suppresses cancer cell proliferation and recent findings have implicated its role as a tumor suppressor. We conducted a chemical library screen to identify nontoxic AhR ligands with anti-cancer effects and discovered flutamide (Eulexin) as a putative AhR ligand. Flutamide is an androgen receptor (AR) antagonist approved by the United States Food and Drug Administration for the treatment of prostate cancer. We found that flutamide inhibited the growth of several cancer cell lines independent of AR status, and that suppression of AhR expression reversed the anti-proliferative effects of flutamide. We investigated the AhR-dependent mechanism of action of flutamide in human hepatocellular carcinoma cells and identified that transforming growth factor-β1 (TGF-β1) is induced by flutamide in an AhR-dependent manner. In contrast, the potent AhR agonist 2,3,7,8-Tetrachlorodibenzo-p-dioxin had no effect on TGF-β1 expression, indicating the ligand specificity of AhR activation. We also determined that TGF-β1 induction is required for the AhR-dependent growth inhibitory effects of flutamide. Therefore, flutamide may be effective in AhR-positive cancers that are sensitive to TGF-β1 signaling, such as hepatocellular carcinoma.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/onc.2015.55</identifier><identifier>PMID: 25867062</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/51 ; 38 ; 631/67 ; 96 ; Androgen Antagonists - pharmacology ; Androgen receptors ; Androgens ; Apoptosis ; Carcinoma, Hepatocellular - drug therapy ; Carcinoma, Hepatocellular - pathology ; Care and treatment ; Cell Biology ; Cell growth ; Cell proliferation ; Cell Proliferation - drug effects ; Cellular signal transduction ; Chemical sensors ; Dioxins ; Flutamide ; Flutamide - pharmacology ; Genetic aspects ; Growth factors ; Health aspects ; Helix-loop-helix proteins (basic) ; Hep G2 Cells ; Hepatocellular carcinoma ; Hepatoma ; Human Genetics ; Humans ; Hydrocarbons ; Internal Medicine ; Ligands ; Liver cancer ; Liver Neoplasms - drug therapy ; Liver Neoplasms - pathology ; Medicine ; Medicine & Public Health ; Oncology ; original-article ; Prostate cancer ; Receptors, Aryl Hydrocarbon - physiology ; Toxicity ; Transforming Growth Factor beta1 - physiology ; Transforming growth factor-b1 ; Transforming growth factors ; Tumor cell lines ; Tumor suppressor genes</subject><ispartof>Oncogene, 2015-12, Vol.34 (50), p.6092-6104</ispartof><rights>Macmillan Publishers Limited 2015</rights><rights>COPYRIGHT 2015 Nature Publishing Group</rights><rights>Macmillan Publishers Limited 2015.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c528t-51bed561112448fca612e0c0e20af835fdbc7b2f9423792e8f6d3f19afa9147c3</citedby><cites>FETCH-LOGICAL-c528t-51bed561112448fca612e0c0e20af835fdbc7b2f9423792e8f6d3f19afa9147c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25867062$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Koch, D C</creatorcontrib><creatorcontrib>Jang, H S</creatorcontrib><creatorcontrib>O'Donnell, E F</creatorcontrib><creatorcontrib>Punj, S</creatorcontrib><creatorcontrib>Kopparapu, P R</creatorcontrib><creatorcontrib>Bisson, W H</creatorcontrib><creatorcontrib>Kerkvliet, N I</creatorcontrib><creatorcontrib>Kolluri, S K</creatorcontrib><title>Anti-androgen flutamide suppresses hepatocellular carcinoma cell proliferation via the aryl hydrocarbon receptor mediated induction of transforming growth factor-β1</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor and a member of the basic helix-loop-helix PER/ARNT/SIM family of chemosensors and developmental regulators. The AhR is widely known as a mediator of dioxin toxicity; however, it also suppresses cancer cell proliferation and recent findings have implicated its role as a tumor suppressor. We conducted a chemical library screen to identify nontoxic AhR ligands with anti-cancer effects and discovered flutamide (Eulexin) as a putative AhR ligand. Flutamide is an androgen receptor (AR) antagonist approved by the United States Food and Drug Administration for the treatment of prostate cancer. We found that flutamide inhibited the growth of several cancer cell lines independent of AR status, and that suppression of AhR expression reversed the anti-proliferative effects of flutamide. We investigated the AhR-dependent mechanism of action of flutamide in human hepatocellular carcinoma cells and identified that transforming growth factor-β1 (TGF-β1) is induced by flutamide in an AhR-dependent manner. In contrast, the potent AhR agonist 2,3,7,8-Tetrachlorodibenzo-p-dioxin had no effect on TGF-β1 expression, indicating the ligand specificity of AhR activation. We also determined that TGF-β1 induction is required for the AhR-dependent growth inhibitory effects of flutamide. Therefore, flutamide may be effective in AhR-positive cancers that are sensitive to TGF-β1 signaling, such as hepatocellular carcinoma.</description><subject>13/51</subject><subject>38</subject><subject>631/67</subject><subject>96</subject><subject>Androgen Antagonists - pharmacology</subject><subject>Androgen receptors</subject><subject>Androgens</subject><subject>Apoptosis</subject><subject>Carcinoma, Hepatocellular - drug therapy</subject><subject>Carcinoma, Hepatocellular - pathology</subject><subject>Care and treatment</subject><subject>Cell Biology</subject><subject>Cell growth</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - drug effects</subject><subject>Cellular signal transduction</subject><subject>Chemical sensors</subject><subject>Dioxins</subject><subject>Flutamide</subject><subject>Flutamide - pharmacology</subject><subject>Genetic aspects</subject><subject>Growth factors</subject><subject>Health aspects</subject><subject>Helix-loop-helix proteins (basic)</subject><subject>Hep G2 Cells</subject><subject>Hepatocellular carcinoma</subject><subject>Hepatoma</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Hydrocarbons</subject><subject>Internal Medicine</subject><subject>Ligands</subject><subject>Liver cancer</subject><subject>Liver Neoplasms - 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In contrast, the potent AhR agonist 2,3,7,8-Tetrachlorodibenzo-p-dioxin had no effect on TGF-β1 expression, indicating the ligand specificity of AhR activation. We also determined that TGF-β1 induction is required for the AhR-dependent growth inhibitory effects of flutamide. Therefore, flutamide may be effective in AhR-positive cancers that are sensitive to TGF-β1 signaling, such as hepatocellular carcinoma.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>25867062</pmid><doi>10.1038/onc.2015.55</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 13/51 38 631/67 96 Androgen Antagonists - pharmacology Androgen receptors Androgens Apoptosis Carcinoma, Hepatocellular - drug therapy Carcinoma, Hepatocellular - pathology Care and treatment Cell Biology Cell growth Cell proliferation Cell Proliferation - drug effects Cellular signal transduction Chemical sensors Dioxins Flutamide Flutamide - pharmacology Genetic aspects Growth factors Health aspects Helix-loop-helix proteins (basic) Hep G2 Cells Hepatocellular carcinoma Hepatoma Human Genetics Humans Hydrocarbons Internal Medicine Ligands Liver cancer Liver Neoplasms - drug therapy Liver Neoplasms - pathology Medicine Medicine & Public Health Oncology original-article Prostate cancer Receptors, Aryl Hydrocarbon - physiology Toxicity Transforming Growth Factor beta1 - physiology Transforming growth factor-b1 Transforming growth factors Tumor cell lines Tumor suppressor genes |
| title | Anti-androgen flutamide suppresses hepatocellular carcinoma cell proliferation via the aryl hydrocarbon receptor mediated induction of transforming growth factor-β1 |
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