Corilagin suppresses cholangiocarcinoma progression through Notch signaling pathway in vitro and in vivo
Corilagin is a natural plant polyphenol tannic acid with antitumor, anti-inflammatory, and anti-oxidative properties. However, the mechanisms of its actions are largely unknown. Our group reported that corilagin could induce cell inhibition in human breast cancer cell line MCF-7 and human liver hepa...
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| Veröffentlicht in: | International journal of oncology 2016-05, Vol.48 (5), p.1868-1876 |
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| creator | GU, YUE XIAO, LINFENG MING, YANLIN ZHENG, ZHIZHONG LI, WENGANG |
| description | Corilagin is a natural plant polyphenol tannic acid with antitumor, anti-inflammatory, and anti-oxidative properties. However, the mechanisms of its actions are largely unknown. Our group reported that corilagin could induce cell inhibition in human breast cancer cell line MCF-7 and human liver hepatocellular carcinoma cell lines HepG2. We report here that corilagin inhibits cholangiocarcinoma (CCA) development through regulating Notch signaling pathway. We found that, in vitro, corilagin inhibited CCA cell proliferation, migration and invasion, promoted CCA cell apoptosis, and inhibited Notch1 and Notch signaling pathway protein expression. Co-immunoprecipitation was used to establish Notch intracellular domain (NICD) interaction with MAML1 and P300 in CCA. Importantly, corilagin reduced Hes1 mRNA level through inhibiting Hes1 promoter activity. In nude mice, corilagin inhibited CCA growth and repressed the expression of Notch1 and mTOR. These results indicate that corilagin may control CCA cell growth by downregulating the expression of Notch1. Therefore, our findings suggest that corilagin may have the potential to become a new therapeutic drug for human CCA. |
| doi_str_mv | 10.3892/ijo.2016.3413 |
| format | Article |
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However, the mechanisms of its actions are largely unknown. Our group reported that corilagin could induce cell inhibition in human breast cancer cell line MCF-7 and human liver hepatocellular carcinoma cell lines HepG2. We report here that corilagin inhibits cholangiocarcinoma (CCA) development through regulating Notch signaling pathway. We found that, in vitro, corilagin inhibited CCA cell proliferation, migration and invasion, promoted CCA cell apoptosis, and inhibited Notch1 and Notch signaling pathway protein expression. Co-immunoprecipitation was used to establish Notch intracellular domain (NICD) interaction with MAML1 and P300 in CCA. Importantly, corilagin reduced Hes1 mRNA level through inhibiting Hes1 promoter activity. In nude mice, corilagin inhibited CCA growth and repressed the expression of Notch1 and mTOR. These results indicate that corilagin may control CCA cell growth by downregulating the expression of Notch1. Therefore, our findings suggest that corilagin may have the potential to become a new therapeutic drug for human CCA.</description><identifier>ISSN: 1019-6439</identifier><identifier>EISSN: 1791-2423</identifier><identifier>DOI: 10.3892/ijo.2016.3413</identifier><identifier>PMID: 26935808</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Animals ; Antineoplastic Agents - administration & dosage ; Antineoplastic Agents - pharmacology ; Apoptosis ; Bile Duct Neoplasms - drug therapy ; Bile Duct Neoplasms - genetics ; Bile Duct Neoplasms - metabolism ; Breast cancer ; Cancer therapies ; Cell growth ; Cell Line, Tumor ; Cell Movement - drug effects ; Cell Proliferation - drug effects ; Cell Survival - drug effects ; Cellular signal transduction ; Chemotherapy ; Chinese medicine ; Cholangiocarcinoma ; Cholangiocarcinoma - drug therapy ; Cholangiocarcinoma - genetics ; Cholangiocarcinoma - metabolism ; corilagin ; Cytotoxicity ; Disease Progression ; Drug resistance ; Gene Expression Regulation, Neoplastic - drug effects ; Genetic aspects ; Glucosides - administration & dosage ; Glucosides - pharmacology ; Health aspects ; Humans ; Hydrolyzable Tannins - administration & dosage ; Hydrolyzable Tannins - pharmacology ; In Vitro Techniques ; invasion ; Medical prognosis ; Messenger RNA ; Mice ; Mice, Nude ; migration ; Notch signaling pathway ; Oxidative stress ; proliferation ; Properties ; Protein expression ; Proteins ; R&D ; Receptors, Notch - metabolism ; Research & development ; Rodents ; Signal Transduction - drug effects ; Studies ; Tannins ; Transcription Factor HES-1 - genetics ; Xenograft Model Antitumor Assays</subject><ispartof>International journal of oncology, 2016-05, Vol.48 (5), p.1868-1876</ispartof><rights>Copyright: © Gu et al.</rights><rights>COPYRIGHT 2016 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2016</rights><rights>Copyright: © Gu et al. 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c545t-678ea7d6b9e102a2be515f6ca734d04b61395fd6116bb4942f37953e88d21f6c3</citedby><cites>FETCH-LOGICAL-c545t-678ea7d6b9e102a2be515f6ca734d04b61395fd6116bb4942f37953e88d21f6c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,5571,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26935808$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>GU, YUE</creatorcontrib><creatorcontrib>XIAO, LINFENG</creatorcontrib><creatorcontrib>MING, YANLIN</creatorcontrib><creatorcontrib>ZHENG, ZHIZHONG</creatorcontrib><creatorcontrib>LI, WENGANG</creatorcontrib><title>Corilagin suppresses cholangiocarcinoma progression through Notch signaling pathway in vitro and in vivo</title><title>International journal of oncology</title><addtitle>Int J Oncol</addtitle><description>Corilagin is a natural plant polyphenol tannic acid with antitumor, anti-inflammatory, and anti-oxidative properties. However, the mechanisms of its actions are largely unknown. Our group reported that corilagin could induce cell inhibition in human breast cancer cell line MCF-7 and human liver hepatocellular carcinoma cell lines HepG2. We report here that corilagin inhibits cholangiocarcinoma (CCA) development through regulating Notch signaling pathway. We found that, in vitro, corilagin inhibited CCA cell proliferation, migration and invasion, promoted CCA cell apoptosis, and inhibited Notch1 and Notch signaling pathway protein expression. Co-immunoprecipitation was used to establish Notch intracellular domain (NICD) interaction with MAML1 and P300 in CCA. Importantly, corilagin reduced Hes1 mRNA level through inhibiting Hes1 promoter activity. In nude mice, corilagin inhibited CCA growth and repressed the expression of Notch1 and mTOR. These results indicate that corilagin may control CCA cell growth by downregulating the expression of Notch1. Therefore, our findings suggest that corilagin may have the potential to become a new therapeutic drug for human CCA.</description><subject>Animals</subject><subject>Antineoplastic Agents - administration & dosage</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Apoptosis</subject><subject>Bile Duct Neoplasms - drug therapy</subject><subject>Bile Duct Neoplasms - genetics</subject><subject>Bile Duct Neoplasms - metabolism</subject><subject>Breast cancer</subject><subject>Cancer therapies</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - drug effects</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Survival - drug effects</subject><subject>Cellular signal transduction</subject><subject>Chemotherapy</subject><subject>Chinese medicine</subject><subject>Cholangiocarcinoma</subject><subject>Cholangiocarcinoma - drug therapy</subject><subject>Cholangiocarcinoma - genetics</subject><subject>Cholangiocarcinoma - metabolism</subject><subject>corilagin</subject><subject>Cytotoxicity</subject><subject>Disease Progression</subject><subject>Drug resistance</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Genetic aspects</subject><subject>Glucosides - administration & dosage</subject><subject>Glucosides - pharmacology</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Hydrolyzable Tannins - administration & dosage</subject><subject>Hydrolyzable Tannins - pharmacology</subject><subject>In Vitro Techniques</subject><subject>invasion</subject><subject>Medical prognosis</subject><subject>Messenger RNA</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>migration</subject><subject>Notch signaling pathway</subject><subject>Oxidative stress</subject><subject>proliferation</subject><subject>Properties</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>R&D</subject><subject>Receptors, Notch - metabolism</subject><subject>Research & development</subject><subject>Rodents</subject><subject>Signal Transduction - drug effects</subject><subject>Studies</subject><subject>Tannins</subject><subject>Transcription Factor HES-1 - genetics</subject><subject>Xenograft Model Antitumor Assays</subject><issn>1019-6439</issn><issn>1791-2423</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkt-L1DAQx4so3g999FUKgj51ze8mL8Kx6Ckc-qLPIU3TNkubqUm7x_33ZtlzvQXJwySZz3xhZr5F8QajDZWKfPQ72BCExYYyTJ8Vl7hWuCKM0Of5jrCqBKPqorhKaYcQ4Rzhl8UFEYpyieRlMWwh-tH0PpRpnefoUnKptAOMJvQerInWB5hMOUfoD1kPoVyGCGs_lN9hsUOZfB_M6ENfzmYZ7s1DmcX2folQmtAeH3t4VbzozJjc68d4Xfz68vnn9mt19-P22_bmrrKc8aUStXSmbkWjHEbEkMZxzDthTU1Zi1gjMFW8awXGommYYqSjteLUSdkSnDl6XXw66s5rM7nWurBEM-o5-snEBw3G6_NM8IPuYa-ZREpwkQXePQpE-L26tOgdrDF3mDRWlFCk6hr9o3ozOu1DB1nMTj5ZfcO4IFIJzDO1-Q-VT-smbyG4zuf_s4L3TwoGZ8ZlSDCuSx57OgerI2gjpBRdd-oQI30whs7G0Adj6IMxMv_26VhO9F8nZODDEUhz3ppvIZ2YrFQxWSFeYSkk_QNFaMGa</recordid><startdate>20160501</startdate><enddate>20160501</enddate><creator>GU, YUE</creator><creator>XIAO, LINFENG</creator><creator>MING, YANLIN</creator><creator>ZHENG, ZHIZHONG</creator><creator>LI, WENGANG</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>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope></search><sort><creationdate>20160501</creationdate><title>Corilagin suppresses cholangiocarcinoma progression through Notch signaling pathway in vitro and in vivo</title><author>GU, YUE ; XIAO, LINFENG ; MING, YANLIN ; ZHENG, ZHIZHONG ; LI, WENGANG</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c545t-678ea7d6b9e102a2be515f6ca734d04b61395fd6116bb4942f37953e88d21f6c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Antineoplastic Agents - 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administration & dosage</topic><topic>Glucosides - pharmacology</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Hydrolyzable Tannins - administration & dosage</topic><topic>Hydrolyzable Tannins - pharmacology</topic><topic>In Vitro Techniques</topic><topic>invasion</topic><topic>Medical prognosis</topic><topic>Messenger RNA</topic><topic>Mice</topic><topic>Mice, Nude</topic><topic>migration</topic><topic>Notch signaling pathway</topic><topic>Oxidative stress</topic><topic>proliferation</topic><topic>Properties</topic><topic>Protein expression</topic><topic>Proteins</topic><topic>R&D</topic><topic>Receptors, Notch - metabolism</topic><topic>Research & development</topic><topic>Rodents</topic><topic>Signal Transduction - drug effects</topic><topic>Studies</topic><topic>Tannins</topic><topic>Transcription Factor HES-1 - genetics</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>GU, YUE</creatorcontrib><creatorcontrib>XIAO, LINFENG</creatorcontrib><creatorcontrib>MING, YANLIN</creatorcontrib><creatorcontrib>ZHENG, ZHIZHONG</creatorcontrib><creatorcontrib>LI, WENGANG</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>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</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>PubMed Central (Full Participant titles)</collection><jtitle>International journal of oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>GU, YUE</au><au>XIAO, LINFENG</au><au>MING, YANLIN</au><au>ZHENG, ZHIZHONG</au><au>LI, WENGANG</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Corilagin suppresses cholangiocarcinoma progression through Notch signaling pathway in vitro and in vivo</atitle><jtitle>International journal of oncology</jtitle><addtitle>Int J Oncol</addtitle><date>2016-05-01</date><risdate>2016</risdate><volume>48</volume><issue>5</issue><spage>1868</spage><epage>1876</epage><pages>1868-1876</pages><issn>1019-6439</issn><eissn>1791-2423</eissn><abstract>Corilagin is a natural plant polyphenol tannic acid with antitumor, anti-inflammatory, and anti-oxidative properties. However, the mechanisms of its actions are largely unknown. Our group reported that corilagin could induce cell inhibition in human breast cancer cell line MCF-7 and human liver hepatocellular carcinoma cell lines HepG2. We report here that corilagin inhibits cholangiocarcinoma (CCA) development through regulating Notch signaling pathway. We found that, in vitro, corilagin inhibited CCA cell proliferation, migration and invasion, promoted CCA cell apoptosis, and inhibited Notch1 and Notch signaling pathway protein expression. Co-immunoprecipitation was used to establish Notch intracellular domain (NICD) interaction with MAML1 and P300 in CCA. Importantly, corilagin reduced Hes1 mRNA level through inhibiting Hes1 promoter activity. In nude mice, corilagin inhibited CCA growth and repressed the expression of Notch1 and mTOR. These results indicate that corilagin may control CCA cell growth by downregulating the expression of Notch1. Therefore, our findings suggest that corilagin may have the potential to become a new therapeutic drug for human CCA.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>26935808</pmid><doi>10.3892/ijo.2016.3413</doi><tpages>9</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 | Animals Antineoplastic Agents - administration & dosage Antineoplastic Agents - pharmacology Apoptosis Bile Duct Neoplasms - drug therapy Bile Duct Neoplasms - genetics Bile Duct Neoplasms - metabolism Breast cancer Cancer therapies Cell growth Cell Line, Tumor Cell Movement - drug effects Cell Proliferation - drug effects Cell Survival - drug effects Cellular signal transduction Chemotherapy Chinese medicine Cholangiocarcinoma Cholangiocarcinoma - drug therapy Cholangiocarcinoma - genetics Cholangiocarcinoma - metabolism corilagin Cytotoxicity Disease Progression Drug resistance Gene Expression Regulation, Neoplastic - drug effects Genetic aspects Glucosides - administration & dosage Glucosides - pharmacology Health aspects Humans Hydrolyzable Tannins - administration & dosage Hydrolyzable Tannins - pharmacology In Vitro Techniques invasion Medical prognosis Messenger RNA Mice Mice, Nude migration Notch signaling pathway Oxidative stress proliferation Properties Protein expression Proteins R&D Receptors, Notch - metabolism Research & development Rodents Signal Transduction - drug effects Studies Tannins Transcription Factor HES-1 - genetics Xenograft Model Antitumor Assays |
| title | Corilagin suppresses cholangiocarcinoma progression through Notch signaling pathway in vitro and in vivo |
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