Berberine targets epidermal growth factor receptor signaling to suppress prostate cancer proliferation in vitro
Berberine is a well-known component of the Chinese herbal medicine Huanglian (Coptis chinensis), and is capable of inhibiting the proliferation of multiple cancer cell lines. However, information available regarding the effect of berberine on prostate cancer cell growth is limited. In the present st...
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| Veröffentlicht in: | Molecular medicine reports 2015-03, Vol.11 (3), p.2125-2128 |
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| creator | HUANG, ZHENG-HUA ZHENG, HONG-FANG WANG, WEI-LU WANG, YONG ZHONG, LONG-FEI WU, JIU-LONG LI, QIAO-XING |
| description | Berberine is a well-known component of the Chinese herbal medicine Huanglian (Coptis chinensis), and is capable of inhibiting the proliferation of multiple cancer cell lines. However, information available regarding the effect of berberine on prostate cancer cell growth is limited. In the present study, LnCaP and PC-3 human prostate cancer cell lines were selected as in vitro models in order to assess the efficacy of berberine as an anticancer agent. A cell proliferation assay demonstrated that berberine inhibited cell growth in a dose-and time-dependent manner. Further investigation revealed berberine significantly accumulated inside cells that were in the G1 phase of the cell cycle and enhanced apoptosis. Western blot analysis demonstrated that berberine inhibited the expression of prostate-specific antigen and the activation of epidermal growth factor receptor (EGFR), and it attenuated EGFR activation following EGF treatment in vitro. In conclusion, the results indicate that berberine inhibits the proliferation of prostate cancer cells through apoptosis and/or cell cycle arrest by inactivation of the EGFR signaling pathway. |
| doi_str_mv | 10.3892/mmr.2014.2929 |
| format | Article |
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However, information available regarding the effect of berberine on prostate cancer cell growth is limited. In the present study, LnCaP and PC-3 human prostate cancer cell lines were selected as in vitro models in order to assess the efficacy of berberine as an anticancer agent. A cell proliferation assay demonstrated that berberine inhibited cell growth in a dose-and time-dependent manner. Further investigation revealed berberine significantly accumulated inside cells that were in the G1 phase of the cell cycle and enhanced apoptosis. Western blot analysis demonstrated that berberine inhibited the expression of prostate-specific antigen and the activation of epidermal growth factor receptor (EGFR), and it attenuated EGFR activation following EGF treatment in vitro. In conclusion, the results indicate that berberine inhibits the proliferation of prostate cancer cells through apoptosis and/or cell cycle arrest by inactivation of the EGFR signaling pathway.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2014.2929</identifier><identifier>PMID: 25394789</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Analysis ; Apoptosis ; Apoptosis - drug effects ; Berberine ; Berberine - pharmacology ; Cancer therapies ; Cell cycle ; Cell Cycle - drug effects ; Cell Cycle Checkpoints - drug effects ; Cell growth ; Cell Line, Tumor ; Cell proliferation ; Cell Proliferation - drug effects ; Cell Survival - drug effects ; Epidermal growth factor ; Epidermal Growth Factor - drug effects ; Epidermal Growth Factor - metabolism ; epidermal growth factor receptor ; Epidermal growth factor receptors ; G1 phase ; Gene Expression ; Herbal medicine ; Homeostasis ; Humans ; Male ; Mortality ; Prevention ; Prostate cancer ; Prostate-specific antigen ; Prostate-Specific Antigen - genetics ; Prostate-Specific Antigen - metabolism ; Prostatic Neoplasms - genetics ; Prostatic Neoplasms - metabolism ; Proteins ; Receptor, Epidermal Growth Factor - metabolism ; Signal transduction ; Signal Transduction - drug effects ; Studies ; Tumor cell lines</subject><ispartof>Molecular medicine reports, 2015-03, Vol.11 (3), p.2125-2128</ispartof><rights>Copyright © 2015, Spandidos Publications</rights><rights>COPYRIGHT 2015 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c525t-716ff9ae1fc1ff0f146933d0e70fcf48435dae17a22dc29bcbab3e1f13ca4fce3</citedby><cites>FETCH-LOGICAL-c525t-716ff9ae1fc1ff0f146933d0e70fcf48435dae17a22dc29bcbab3e1f13ca4fce3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,5571,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25394789$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>HUANG, ZHENG-HUA</creatorcontrib><creatorcontrib>ZHENG, HONG-FANG</creatorcontrib><creatorcontrib>WANG, WEI-LU</creatorcontrib><creatorcontrib>WANG, YONG</creatorcontrib><creatorcontrib>ZHONG, LONG-FEI</creatorcontrib><creatorcontrib>WU, JIU-LONG</creatorcontrib><creatorcontrib>LI, QIAO-XING</creatorcontrib><title>Berberine targets epidermal growth factor receptor signaling to suppress prostate cancer proliferation in vitro</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Berberine is a well-known component of the Chinese herbal medicine Huanglian (Coptis chinensis), and is capable of inhibiting the proliferation of multiple cancer cell lines. However, information available regarding the effect of berberine on prostate cancer cell growth is limited. In the present study, LnCaP and PC-3 human prostate cancer cell lines were selected as in vitro models in order to assess the efficacy of berberine as an anticancer agent. A cell proliferation assay demonstrated that berberine inhibited cell growth in a dose-and time-dependent manner. Further investigation revealed berberine significantly accumulated inside cells that were in the G1 phase of the cell cycle and enhanced apoptosis. Western blot analysis demonstrated that berberine inhibited the expression of prostate-specific antigen and the activation of epidermal growth factor receptor (EGFR), and it attenuated EGFR activation following EGF treatment in vitro. In conclusion, the results indicate that berberine inhibits the proliferation of prostate cancer cells through apoptosis and/or cell cycle arrest by inactivation of the EGFR signaling pathway.</description><subject>Analysis</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Berberine</subject><subject>Berberine - pharmacology</subject><subject>Cancer therapies</subject><subject>Cell cycle</subject><subject>Cell Cycle - drug effects</subject><subject>Cell Cycle Checkpoints - drug effects</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Survival - drug effects</subject><subject>Epidermal growth factor</subject><subject>Epidermal Growth Factor - drug effects</subject><subject>Epidermal Growth Factor - metabolism</subject><subject>epidermal growth factor receptor</subject><subject>Epidermal growth factor receptors</subject><subject>G1 phase</subject><subject>Gene Expression</subject><subject>Herbal medicine</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Male</subject><subject>Mortality</subject><subject>Prevention</subject><subject>Prostate cancer</subject><subject>Prostate-specific antigen</subject><subject>Prostate-Specific Antigen - genetics</subject><subject>Prostate-Specific Antigen - metabolism</subject><subject>Prostatic Neoplasms - genetics</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>Proteins</subject><subject>Receptor, Epidermal Growth Factor - metabolism</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Studies</subject><subject>Tumor cell lines</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptkUtv1TAQhSNERUthyRZZYkE3ufiV5HrZVjwqVeqmrC3HGQdXiR3GThH_Hkf3UgRCXnjG_ubo2Keq3jC6E3vFP8wz7jhlcscVV8-qM9YpVgtK5fNjzZXqTquXKT1Q2ja8US-qU94IJbu9OqviFWAP6AOQbHCEnAgsfgCczURGjD_yN-KMzREJgoVlK5Ifg5l8GEmOJK3LgpASWTCmbDIQa4IF3PrJO0CTfQzEB_LoM8ZX1YkzU4LXx_28-vrp4_31l_r27vPN9eVtbYvFXHesdU4ZYM4y56hjslVCDBQ66qyTeymaodx2hvPBctXb3vSi0ExYI50FcV5dHHSLje8rpKxnnyxMkwkQ16RZK2THG0mbgr77B32IK5YXFkoJLttOKfmHGs0E2gcXMxq7iepLSfdtUWtpoXb_ocoaYPY2BnC-nP81UB8GbPm-hOD0gn42-FMzqreAdQlYbwHrLeDCvz2aXfsZhif6d6IFeH8A0mLC4IeYnpiiVDNWU1FzVvhfPouv4w</recordid><startdate>20150301</startdate><enddate>20150301</enddate><creator>HUANG, ZHENG-HUA</creator><creator>ZHENG, HONG-FANG</creator><creator>WANG, WEI-LU</creator><creator>WANG, YONG</creator><creator>ZHONG, LONG-FEI</creator><creator>WU, JIU-LONG</creator><creator>LI, QIAO-XING</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20150301</creationdate><title>Berberine targets epidermal growth factor receptor signaling to suppress prostate cancer proliferation in vitro</title><author>HUANG, ZHENG-HUA ; ZHENG, HONG-FANG ; WANG, WEI-LU ; WANG, YONG ; ZHONG, LONG-FEI ; WU, JIU-LONG ; LI, QIAO-XING</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c525t-716ff9ae1fc1ff0f146933d0e70fcf48435dae17a22dc29bcbab3e1f13ca4fce3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Analysis</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Berberine</topic><topic>Berberine - pharmacology</topic><topic>Cancer therapies</topic><topic>Cell cycle</topic><topic>Cell Cycle - drug effects</topic><topic>Cell Cycle Checkpoints - drug effects</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell Survival - drug effects</topic><topic>Epidermal growth factor</topic><topic>Epidermal Growth Factor - drug effects</topic><topic>Epidermal Growth Factor - metabolism</topic><topic>epidermal growth factor receptor</topic><topic>Epidermal growth factor receptors</topic><topic>G1 phase</topic><topic>Gene Expression</topic><topic>Herbal medicine</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>Male</topic><topic>Mortality</topic><topic>Prevention</topic><topic>Prostate cancer</topic><topic>Prostate-specific antigen</topic><topic>Prostate-Specific Antigen - genetics</topic><topic>Prostate-Specific Antigen - metabolism</topic><topic>Prostatic Neoplasms - genetics</topic><topic>Prostatic Neoplasms - metabolism</topic><topic>Proteins</topic><topic>Receptor, Epidermal Growth Factor - metabolism</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>Studies</topic><topic>Tumor cell lines</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>HUANG, ZHENG-HUA</creatorcontrib><creatorcontrib>ZHENG, HONG-FANG</creatorcontrib><creatorcontrib>WANG, WEI-LU</creatorcontrib><creatorcontrib>WANG, YONG</creatorcontrib><creatorcontrib>ZHONG, LONG-FEI</creatorcontrib><creatorcontrib>WU, JIU-LONG</creatorcontrib><creatorcontrib>LI, QIAO-XING</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>HUANG, ZHENG-HUA</au><au>ZHENG, HONG-FANG</au><au>WANG, WEI-LU</au><au>WANG, YONG</au><au>ZHONG, LONG-FEI</au><au>WU, JIU-LONG</au><au>LI, QIAO-XING</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Berberine targets epidermal growth factor receptor signaling to suppress prostate cancer proliferation in vitro</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2015-03-01</date><risdate>2015</risdate><volume>11</volume><issue>3</issue><spage>2125</spage><epage>2128</epage><pages>2125-2128</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Berberine is a well-known component of the Chinese herbal medicine Huanglian (Coptis chinensis), and is capable of inhibiting the proliferation of multiple cancer cell lines. However, information available regarding the effect of berberine on prostate cancer cell growth is limited. In the present study, LnCaP and PC-3 human prostate cancer cell lines were selected as in vitro models in order to assess the efficacy of berberine as an anticancer agent. A cell proliferation assay demonstrated that berberine inhibited cell growth in a dose-and time-dependent manner. Further investigation revealed berberine significantly accumulated inside cells that were in the G1 phase of the cell cycle and enhanced apoptosis. Western blot analysis demonstrated that berberine inhibited the expression of prostate-specific antigen and the activation of epidermal growth factor receptor (EGFR), and it attenuated EGFR activation following EGF treatment in vitro. In conclusion, the results indicate that berberine inhibits the proliferation of prostate cancer cells through apoptosis and/or cell cycle arrest by inactivation of the EGFR signaling pathway.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>25394789</pmid><doi>10.3892/mmr.2014.2929</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Analysis Apoptosis Apoptosis - drug effects Berberine Berberine - pharmacology Cancer therapies Cell cycle Cell Cycle - drug effects Cell Cycle Checkpoints - drug effects Cell growth Cell Line, Tumor Cell proliferation Cell Proliferation - drug effects Cell Survival - drug effects Epidermal growth factor Epidermal Growth Factor - drug effects Epidermal Growth Factor - metabolism epidermal growth factor receptor Epidermal growth factor receptors G1 phase Gene Expression Herbal medicine Homeostasis Humans Male Mortality Prevention Prostate cancer Prostate-specific antigen Prostate-Specific Antigen - genetics Prostate-Specific Antigen - metabolism Prostatic Neoplasms - genetics Prostatic Neoplasms - metabolism Proteins Receptor, Epidermal Growth Factor - metabolism Signal transduction Signal Transduction - drug effects Studies Tumor cell lines |
| title | Berberine targets epidermal growth factor receptor signaling to suppress prostate cancer proliferation in vitro |
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