Hepatic Stellate Cells Accelerate the Malignant Behavior of Cholangiocarcinoma Cells
Background Although tumor–stromal interaction has been discussed, the role of hepatic stellate (HS) cells against cancer, especially cholangiocarcinoma (CC), has not been clarified. The aim of this study is to investigate the effect of HS cells on CC cell progression in vitro and in vivo. Methods Th...
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| Veröffentlicht in: | Annals of surgical oncology 2011-04, Vol.18 (4), p.1175-1184 |
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| creator | Okabe, Hirohisa Beppu, Toru Hayashi, Hiromitsu Ishiko, Takatoshi Masuda, Toshiro Otao, Ryu Horlad, Hasita Jono, Hirohumi Ueda, Mitsuharu PhD, Satoru Shinriki Ando, Yukio Baba, Hideo |
| description | Background
Although tumor–stromal interaction has been discussed, the role of hepatic stellate (HS) cells against cancer, especially cholangiocarcinoma (CC), has not been clarified. The aim of this study is to investigate the effect of HS cells on CC cell progression in vitro and in vivo.
Methods
The effects of CC conditioned medium (CC-CM) on activation and proliferation of HS cells (LI90 and LX-2), the influences of HS cell CM (HS-CM) on proliferation and invasion of CC cells (HuCCT-1 and RBE), and the effects of their interaction on HUVEC tube formation were assessed using each CM. The effect of HS cells on tumor growth was examined in vivo by subcutaneous co-injection. Cytokine array was performed to assess the secreted proteins induced by their coculture.
Results
CC-CM activated HS cells and increased their proliferation. HS-CM dose-dependently increased CC cell proliferation and invasion. Chemotherapy of CC cells was less effective when treated with HS-CM. HS-CM activated the mitogen-activated protein kinase and Akt pathways in tumor cells. The indirect interaction of CC and HS cells promotes tube formation of human umbilical venous endothelial cells. Subcutaneous co-injection of tumor cells with HS cells in nude mouse resulted in increased tumor size. Several proteins were found in the culture medium induced by their coculture, thought to be key proteins which regulated tumor–stromal interaction.
Conclusions
This study indicates that HS cells play an important role in accelerating cholangiocarcinoma progression and may be a therapeutic target in cholangiocarcinoma. |
| doi_str_mv | 10.1245/s10434-010-1391-7 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_856766356</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>856766356</sourcerecordid><originalsourceid>FETCH-LOGICAL-c436t-21494e4cafb3a0ded98c5daf65843d9890d084970d160090f16e03d2d33d76a33</originalsourceid><addsrcrecordid>eNp1kMtOwzAQRS0EoqXwAWxQxIZVYPxMsiwRL6mIBWUdubbTpkriYidI_D2OUkBCYjWe8bl37IvQOYZrTBi_8RgYZTFgiDHNcJwcoCnmYcJEig_DGUQaZ0TwCTrxfguAEwr8GE1IEJKMpVO0fDQ72VUqeu1MXcvORHmoPporZWrjhkG3MdGzrKt1K9suujUb-VFZF9kyyje2lu26sko6VbW2kaP6FB2VsvbmbF9n6O3-bpk_xouXh6d8vogVo6KLCWYZM0zJckUlaKOzVHEtS8FTRkOTgYaUZQloLAAyKLEwQDXRlOpESEpn6Gr03Tn73hvfFU3l1fCP1tjeFykXiRCUi0Be_iG3tndteNwA4UQQMtjhEVLOeu9MWexc1Uj3WWAohsCLMfAChj4EXiRBc7E37leN0T-K74QDQEbAh6t2bdzv5v9dvwBAj4nZ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>856176223</pqid></control><display><type>article</type><title>Hepatic Stellate Cells Accelerate the Malignant Behavior of Cholangiocarcinoma Cells</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Okabe, Hirohisa ; Beppu, Toru ; Hayashi, Hiromitsu ; Ishiko, Takatoshi ; Masuda, Toshiro ; Otao, Ryu ; Horlad, Hasita ; Jono, Hirohumi ; Ueda, Mitsuharu ; PhD, Satoru Shinriki ; Ando, Yukio ; Baba, Hideo</creator><creatorcontrib>Okabe, Hirohisa ; Beppu, Toru ; Hayashi, Hiromitsu ; Ishiko, Takatoshi ; Masuda, Toshiro ; Otao, Ryu ; Horlad, Hasita ; Jono, Hirohumi ; Ueda, Mitsuharu ; PhD, Satoru Shinriki ; Ando, Yukio ; Baba, Hideo</creatorcontrib><description>Background
Although tumor–stromal interaction has been discussed, the role of hepatic stellate (HS) cells against cancer, especially cholangiocarcinoma (CC), has not been clarified. The aim of this study is to investigate the effect of HS cells on CC cell progression in vitro and in vivo.
Methods
The effects of CC conditioned medium (CC-CM) on activation and proliferation of HS cells (LI90 and LX-2), the influences of HS cell CM (HS-CM) on proliferation and invasion of CC cells (HuCCT-1 and RBE), and the effects of their interaction on HUVEC tube formation were assessed using each CM. The effect of HS cells on tumor growth was examined in vivo by subcutaneous co-injection. Cytokine array was performed to assess the secreted proteins induced by their coculture.
Results
CC-CM activated HS cells and increased their proliferation. HS-CM dose-dependently increased CC cell proliferation and invasion. Chemotherapy of CC cells was less effective when treated with HS-CM. HS-CM activated the mitogen-activated protein kinase and Akt pathways in tumor cells. The indirect interaction of CC and HS cells promotes tube formation of human umbilical venous endothelial cells. Subcutaneous co-injection of tumor cells with HS cells in nude mouse resulted in increased tumor size. Several proteins were found in the culture medium induced by their coculture, thought to be key proteins which regulated tumor–stromal interaction.
Conclusions
This study indicates that HS cells play an important role in accelerating cholangiocarcinoma progression and may be a therapeutic target in cholangiocarcinoma.</description><identifier>ISSN: 1068-9265</identifier><identifier>EISSN: 1534-4681</identifier><identifier>DOI: 10.1245/s10434-010-1391-7</identifier><identifier>PMID: 21042948</identifier><language>eng</language><publisher>New York: Springer-Verlag</publisher><subject>Animals ; Antineoplastic Agents - pharmacology ; Apoptosis - drug effects ; Bile Duct Neoplasms - drug therapy ; Bile Duct Neoplasms - metabolism ; Bile Duct Neoplasms - pathology ; Bile Ducts, Intrahepatic - drug effects ; Bile Ducts, Intrahepatic - metabolism ; Bile Ducts, Intrahepatic - pathology ; Blotting, Western ; Cell Adhesion - drug effects ; Cell Movement - drug effects ; Cell Proliferation - drug effects ; Cells, Cultured ; Cholangiocarcinoma - drug therapy ; Cholangiocarcinoma - metabolism ; Cholangiocarcinoma - pathology ; Culture Media, Conditioned - pharmacology ; Cytokines - genetics ; Cytokines - metabolism ; Disease Progression ; Female ; Hepatic Stellate Cells - metabolism ; Hepatic Stellate Cells - pathology ; Humans ; Immunoenzyme Techniques ; Medicine ; Medicine & Public Health ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Mitogen-Activated Protein Kinases - genetics ; Mitogen-Activated Protein Kinases - metabolism ; Oncology ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - genetics ; Surgery ; Surgical Oncology ; Translational Research and Biomarkers</subject><ispartof>Annals of surgical oncology, 2011-04, Vol.18 (4), p.1175-1184</ispartof><rights>Society of Surgical Oncology 2010</rights><rights>Society of Surgical Oncology 2011</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c436t-21494e4cafb3a0ded98c5daf65843d9890d084970d160090f16e03d2d33d76a33</citedby><cites>FETCH-LOGICAL-c436t-21494e4cafb3a0ded98c5daf65843d9890d084970d160090f16e03d2d33d76a33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1245/s10434-010-1391-7$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1245/s10434-010-1391-7$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>315,781,785,27925,27926,41489,42558,51320</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21042948$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Okabe, Hirohisa</creatorcontrib><creatorcontrib>Beppu, Toru</creatorcontrib><creatorcontrib>Hayashi, Hiromitsu</creatorcontrib><creatorcontrib>Ishiko, Takatoshi</creatorcontrib><creatorcontrib>Masuda, Toshiro</creatorcontrib><creatorcontrib>Otao, Ryu</creatorcontrib><creatorcontrib>Horlad, Hasita</creatorcontrib><creatorcontrib>Jono, Hirohumi</creatorcontrib><creatorcontrib>Ueda, Mitsuharu</creatorcontrib><creatorcontrib>PhD, Satoru Shinriki</creatorcontrib><creatorcontrib>Ando, Yukio</creatorcontrib><creatorcontrib>Baba, Hideo</creatorcontrib><title>Hepatic Stellate Cells Accelerate the Malignant Behavior of Cholangiocarcinoma Cells</title><title>Annals of surgical oncology</title><addtitle>Ann Surg Oncol</addtitle><addtitle>Ann Surg Oncol</addtitle><description>Background
Although tumor–stromal interaction has been discussed, the role of hepatic stellate (HS) cells against cancer, especially cholangiocarcinoma (CC), has not been clarified. The aim of this study is to investigate the effect of HS cells on CC cell progression in vitro and in vivo.
Methods
The effects of CC conditioned medium (CC-CM) on activation and proliferation of HS cells (LI90 and LX-2), the influences of HS cell CM (HS-CM) on proliferation and invasion of CC cells (HuCCT-1 and RBE), and the effects of their interaction on HUVEC tube formation were assessed using each CM. The effect of HS cells on tumor growth was examined in vivo by subcutaneous co-injection. Cytokine array was performed to assess the secreted proteins induced by their coculture.
Results
CC-CM activated HS cells and increased their proliferation. HS-CM dose-dependently increased CC cell proliferation and invasion. Chemotherapy of CC cells was less effective when treated with HS-CM. HS-CM activated the mitogen-activated protein kinase and Akt pathways in tumor cells. The indirect interaction of CC and HS cells promotes tube formation of human umbilical venous endothelial cells. Subcutaneous co-injection of tumor cells with HS cells in nude mouse resulted in increased tumor size. Several proteins were found in the culture medium induced by their coculture, thought to be key proteins which regulated tumor–stromal interaction.
Conclusions
This study indicates that HS cells play an important role in accelerating cholangiocarcinoma progression and may be a therapeutic target in cholangiocarcinoma.</description><subject>Animals</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Apoptosis - drug effects</subject><subject>Bile Duct Neoplasms - drug therapy</subject><subject>Bile Duct Neoplasms - metabolism</subject><subject>Bile Duct Neoplasms - pathology</subject><subject>Bile Ducts, Intrahepatic - drug effects</subject><subject>Bile Ducts, Intrahepatic - metabolism</subject><subject>Bile Ducts, Intrahepatic - pathology</subject><subject>Blotting, Western</subject><subject>Cell Adhesion - drug effects</subject><subject>Cell Movement - drug effects</subject><subject>Cell Proliferation - drug effects</subject><subject>Cells, Cultured</subject><subject>Cholangiocarcinoma - drug therapy</subject><subject>Cholangiocarcinoma - metabolism</subject><subject>Cholangiocarcinoma - pathology</subject><subject>Culture Media, Conditioned - pharmacology</subject><subject>Cytokines - genetics</subject><subject>Cytokines - metabolism</subject><subject>Disease Progression</subject><subject>Female</subject><subject>Hepatic Stellate Cells - metabolism</subject><subject>Hepatic Stellate Cells - pathology</subject><subject>Humans</subject><subject>Immunoenzyme Techniques</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Mitogen-Activated Protein Kinases - genetics</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>Oncology</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - genetics</subject><subject>Surgery</subject><subject>Surgical Oncology</subject><subject>Translational Research and Biomarkers</subject><issn>1068-9265</issn><issn>1534-4681</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kMtOwzAQRS0EoqXwAWxQxIZVYPxMsiwRL6mIBWUdubbTpkriYidI_D2OUkBCYjWe8bl37IvQOYZrTBi_8RgYZTFgiDHNcJwcoCnmYcJEig_DGUQaZ0TwCTrxfguAEwr8GE1IEJKMpVO0fDQ72VUqeu1MXcvORHmoPporZWrjhkG3MdGzrKt1K9suujUb-VFZF9kyyje2lu26sko6VbW2kaP6FB2VsvbmbF9n6O3-bpk_xouXh6d8vogVo6KLCWYZM0zJckUlaKOzVHEtS8FTRkOTgYaUZQloLAAyKLEwQDXRlOpESEpn6Gr03Tn73hvfFU3l1fCP1tjeFykXiRCUi0Be_iG3tndteNwA4UQQMtjhEVLOeu9MWexc1Uj3WWAohsCLMfAChj4EXiRBc7E37leN0T-K74QDQEbAh6t2bdzv5v9dvwBAj4nZ</recordid><startdate>20110401</startdate><enddate>20110401</enddate><creator>Okabe, Hirohisa</creator><creator>Beppu, Toru</creator><creator>Hayashi, Hiromitsu</creator><creator>Ishiko, Takatoshi</creator><creator>Masuda, Toshiro</creator><creator>Otao, Ryu</creator><creator>Horlad, Hasita</creator><creator>Jono, Hirohumi</creator><creator>Ueda, Mitsuharu</creator><creator>PhD, Satoru Shinriki</creator><creator>Ando, Yukio</creator><creator>Baba, Hideo</creator><general>Springer-Verlag</general><general>Springer Nature B.V</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>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20110401</creationdate><title>Hepatic Stellate Cells Accelerate the Malignant Behavior of Cholangiocarcinoma Cells</title><author>Okabe, Hirohisa ; Beppu, Toru ; Hayashi, Hiromitsu ; Ishiko, Takatoshi ; Masuda, Toshiro ; Otao, Ryu ; Horlad, Hasita ; Jono, Hirohumi ; Ueda, Mitsuharu ; PhD, Satoru Shinriki ; Ando, Yukio ; Baba, Hideo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c436t-21494e4cafb3a0ded98c5daf65843d9890d084970d160090f16e03d2d33d76a33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Apoptosis - drug effects</topic><topic>Bile Duct Neoplasms - drug therapy</topic><topic>Bile Duct Neoplasms - metabolism</topic><topic>Bile Duct Neoplasms - pathology</topic><topic>Bile Ducts, Intrahepatic - drug effects</topic><topic>Bile Ducts, Intrahepatic - metabolism</topic><topic>Bile Ducts, Intrahepatic - pathology</topic><topic>Blotting, Western</topic><topic>Cell Adhesion - drug effects</topic><topic>Cell Movement - drug effects</topic><topic>Cell Proliferation - drug effects</topic><topic>Cells, Cultured</topic><topic>Cholangiocarcinoma - drug therapy</topic><topic>Cholangiocarcinoma - metabolism</topic><topic>Cholangiocarcinoma - pathology</topic><topic>Culture Media, Conditioned - pharmacology</topic><topic>Cytokines - genetics</topic><topic>Cytokines - metabolism</topic><topic>Disease Progression</topic><topic>Female</topic><topic>Hepatic Stellate Cells - metabolism</topic><topic>Hepatic Stellate Cells - pathology</topic><topic>Humans</topic><topic>Immunoenzyme Techniques</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>Mitogen-Activated Protein Kinases - genetics</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>Oncology</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - genetics</topic><topic>Surgery</topic><topic>Surgical Oncology</topic><topic>Translational Research and Biomarkers</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Okabe, Hirohisa</creatorcontrib><creatorcontrib>Beppu, Toru</creatorcontrib><creatorcontrib>Hayashi, Hiromitsu</creatorcontrib><creatorcontrib>Ishiko, Takatoshi</creatorcontrib><creatorcontrib>Masuda, Toshiro</creatorcontrib><creatorcontrib>Otao, Ryu</creatorcontrib><creatorcontrib>Horlad, Hasita</creatorcontrib><creatorcontrib>Jono, Hirohumi</creatorcontrib><creatorcontrib>Ueda, Mitsuharu</creatorcontrib><creatorcontrib>PhD, Satoru Shinriki</creatorcontrib><creatorcontrib>Ando, Yukio</creatorcontrib><creatorcontrib>Baba, Hideo</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>Oncogenes and Growth Factors Abstracts</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>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>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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>Annals of surgical oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Okabe, Hirohisa</au><au>Beppu, Toru</au><au>Hayashi, Hiromitsu</au><au>Ishiko, Takatoshi</au><au>Masuda, Toshiro</au><au>Otao, Ryu</au><au>Horlad, Hasita</au><au>Jono, Hirohumi</au><au>Ueda, Mitsuharu</au><au>PhD, Satoru Shinriki</au><au>Ando, Yukio</au><au>Baba, Hideo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hepatic Stellate Cells Accelerate the Malignant Behavior of Cholangiocarcinoma Cells</atitle><jtitle>Annals of surgical oncology</jtitle><stitle>Ann Surg Oncol</stitle><addtitle>Ann Surg Oncol</addtitle><date>2011-04-01</date><risdate>2011</risdate><volume>18</volume><issue>4</issue><spage>1175</spage><epage>1184</epage><pages>1175-1184</pages><issn>1068-9265</issn><eissn>1534-4681</eissn><abstract>Background
Although tumor–stromal interaction has been discussed, the role of hepatic stellate (HS) cells against cancer, especially cholangiocarcinoma (CC), has not been clarified. The aim of this study is to investigate the effect of HS cells on CC cell progression in vitro and in vivo.
Methods
The effects of CC conditioned medium (CC-CM) on activation and proliferation of HS cells (LI90 and LX-2), the influences of HS cell CM (HS-CM) on proliferation and invasion of CC cells (HuCCT-1 and RBE), and the effects of their interaction on HUVEC tube formation were assessed using each CM. The effect of HS cells on tumor growth was examined in vivo by subcutaneous co-injection. Cytokine array was performed to assess the secreted proteins induced by their coculture.
Results
CC-CM activated HS cells and increased their proliferation. HS-CM dose-dependently increased CC cell proliferation and invasion. Chemotherapy of CC cells was less effective when treated with HS-CM. HS-CM activated the mitogen-activated protein kinase and Akt pathways in tumor cells. The indirect interaction of CC and HS cells promotes tube formation of human umbilical venous endothelial cells. Subcutaneous co-injection of tumor cells with HS cells in nude mouse resulted in increased tumor size. Several proteins were found in the culture medium induced by their coculture, thought to be key proteins which regulated tumor–stromal interaction.
Conclusions
This study indicates that HS cells play an important role in accelerating cholangiocarcinoma progression and may be a therapeutic target in cholangiocarcinoma.</abstract><cop>New York</cop><pub>Springer-Verlag</pub><pmid>21042948</pmid><doi>10.1245/s10434-010-1391-7</doi><tpages>10</tpages></addata></record> |
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| ispartof | Annals of surgical oncology, 2011-04, Vol.18 (4), p.1175-1184 |
| issn | 1068-9265 1534-4681 |
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| subjects | Animals Antineoplastic Agents - pharmacology Apoptosis - drug effects Bile Duct Neoplasms - drug therapy Bile Duct Neoplasms - metabolism Bile Duct Neoplasms - pathology Bile Ducts, Intrahepatic - drug effects Bile Ducts, Intrahepatic - metabolism Bile Ducts, Intrahepatic - pathology Blotting, Western Cell Adhesion - drug effects Cell Movement - drug effects Cell Proliferation - drug effects Cells, Cultured Cholangiocarcinoma - drug therapy Cholangiocarcinoma - metabolism Cholangiocarcinoma - pathology Culture Media, Conditioned - pharmacology Cytokines - genetics Cytokines - metabolism Disease Progression Female Hepatic Stellate Cells - metabolism Hepatic Stellate Cells - pathology Humans Immunoenzyme Techniques Medicine Medicine & Public Health Mice Mice, Inbred BALB C Mice, Nude Mitogen-Activated Protein Kinases - genetics Mitogen-Activated Protein Kinases - metabolism Oncology Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - genetics Surgery Surgical Oncology Translational Research and Biomarkers |
| title | Hepatic Stellate Cells Accelerate the Malignant Behavior of Cholangiocarcinoma Cells |
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