Tumor-Associated Macrophage Promotes Tumor Progression via STAT3 Signaling in Hepatocellular Carcinoma
Objective: Signal transducer and activator of transcription 3 (STAT3) is activated in hepatocellular carcinoma (HCC), and tumor-associated macrophage plays an important role in tumor progression. Therefore, we examined STAT3 activation, cytokine expression and infiltration of tumor-associated macrop...
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| Veröffentlicht in: | Pathobiology (Basel) 2013-01, Vol.80 (3), p.146-154 |
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| creator | Mano, Yohei Aishima, Shinichi Fujita, Nobuhiro Tanaka, Yuki Kubo, Yuichiro Motomura, Takashi Taketomi, Akinobu Shirabe, Ken Maehara, Yoshihiko Oda, Yoshinao |
| description | Objective: Signal transducer and activator of transcription 3 (STAT3) is activated in hepatocellular carcinoma (HCC), and tumor-associated macrophage plays an important role in tumor progression. Therefore, we examined STAT3 activation, cytokine expression and infiltration of tumor-associated macrophages in resected HCCs as well as the alteration of cell growth and migration by cytokine stimulation in HCC cell lines. Methods: Immunohistochemical staining of phosphorylated STAT3 (pSTAT3), CD163, interleukin (IL)-6, Ki-67 and Bcl-XL was performed for 101 cases of resected HCC, and correlations between pSTAT3 staining and clinicopathological findings were analyzed. In HCC cell lines (PLC/PRF/5 and Huh7), cell proliferation and migration by IL-6 stimulation and S3I-201 (STAT3 inhibitor) treatment were analyzed. Results: In HCC specimens, the pSTAT3-positive group showed high levels of α-fetoprotein (p = 0.0276), large tumor size (p = 0.0092), frequent intrahepatic metastasis (p = 0.0214), high Ki-67 (p = 0.0002) and Bcl-XL (p = 0.0001), poor prognosis (p = 0.0234), and high recurrence rate (p = 0.0003). CD163-positive cells were frequently observed in the pSTAT3-positive group (p = 0.0013). In two HCC cell lines, IL-6 stimulation promoted cell proliferation and migration via the STAT3 phosphorylation, and S3I-201 inhibited this activation. Conclusions: STAT3 activation was correlated with aggressive behavior of HCC and may be mediated via tumor-associated macrophage. We expect that STAT3 signaling and tumor-associated macrophages can be attractive therapeutic targets in HCC patients. |
| doi_str_mv | 10.1159/000346196 |
| format | Article |
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Therefore, we examined STAT3 activation, cytokine expression and infiltration of tumor-associated macrophages in resected HCCs as well as the alteration of cell growth and migration by cytokine stimulation in HCC cell lines. Methods: Immunohistochemical staining of phosphorylated STAT3 (pSTAT3), CD163, interleukin (IL)-6, Ki-67 and Bcl-XL was performed for 101 cases of resected HCC, and correlations between pSTAT3 staining and clinicopathological findings were analyzed. In HCC cell lines (PLC/PRF/5 and Huh7), cell proliferation and migration by IL-6 stimulation and S3I-201 (STAT3 inhibitor) treatment were analyzed. Results: In HCC specimens, the pSTAT3-positive group showed high levels of α-fetoprotein (p = 0.0276), large tumor size (p = 0.0092), frequent intrahepatic metastasis (p = 0.0214), high Ki-67 (p = 0.0002) and Bcl-XL (p = 0.0001), poor prognosis (p = 0.0234), and high recurrence rate (p = 0.0003). CD163-positive cells were frequently observed in the pSTAT3-positive group (p = 0.0013). In two HCC cell lines, IL-6 stimulation promoted cell proliferation and migration via the STAT3 phosphorylation, and S3I-201 inhibited this activation. Conclusions: STAT3 activation was correlated with aggressive behavior of HCC and may be mediated via tumor-associated macrophage. We expect that STAT3 signaling and tumor-associated macrophages can be attractive therapeutic targets in HCC patients.</description><identifier>ISSN: 1015-2008</identifier><identifier>EISSN: 1423-0291</identifier><identifier>DOI: 10.1159/000346196</identifier><identifier>PMID: 23364389</identifier><identifier>CODEN: PATHEF</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Cancer therapies ; Carcinoma, Hepatocellular - immunology ; Carcinoma, Hepatocellular - metabolism ; Carcinoma, Hepatocellular - pathology ; Disease Progression ; Female ; Humans ; Immunoblotting ; Immunohistochemistry ; Liver cancer ; Liver Neoplasms - immunology ; Liver Neoplasms - metabolism ; Liver Neoplasms - pathology ; Macrophages - immunology ; Macrophages - metabolism ; Male ; Metastasis ; Middle Aged ; Original Paper ; Pathology ; Signal Transduction - physiology ; STAT3 Transcription Factor - metabolism ; Tumors</subject><ispartof>Pathobiology (Basel), 2013-01, Vol.80 (3), p.146-154</ispartof><rights>2013 S. Karger AG, Basel</rights><rights>Copyright © 2013 S. Karger AG, Basel.</rights><rights>Copyright (c) 2013 S. Karger AG, Basel</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c464t-b51ebc2dc375f80300ed34668af4fb1007b1ac6947ae67148d2bcc4bab9b57233</citedby><cites>FETCH-LOGICAL-c464t-b51ebc2dc375f80300ed34668af4fb1007b1ac6947ae67148d2bcc4bab9b57233</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,2423,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23364389$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mano, Yohei</creatorcontrib><creatorcontrib>Aishima, Shinichi</creatorcontrib><creatorcontrib>Fujita, Nobuhiro</creatorcontrib><creatorcontrib>Tanaka, Yuki</creatorcontrib><creatorcontrib>Kubo, Yuichiro</creatorcontrib><creatorcontrib>Motomura, Takashi</creatorcontrib><creatorcontrib>Taketomi, Akinobu</creatorcontrib><creatorcontrib>Shirabe, Ken</creatorcontrib><creatorcontrib>Maehara, Yoshihiko</creatorcontrib><creatorcontrib>Oda, Yoshinao</creatorcontrib><title>Tumor-Associated Macrophage Promotes Tumor Progression via STAT3 Signaling in Hepatocellular Carcinoma</title><title>Pathobiology (Basel)</title><addtitle>Pathobiology</addtitle><description>Objective: Signal transducer and activator of transcription 3 (STAT3) is activated in hepatocellular carcinoma (HCC), and tumor-associated macrophage plays an important role in tumor progression. Therefore, we examined STAT3 activation, cytokine expression and infiltration of tumor-associated macrophages in resected HCCs as well as the alteration of cell growth and migration by cytokine stimulation in HCC cell lines. Methods: Immunohistochemical staining of phosphorylated STAT3 (pSTAT3), CD163, interleukin (IL)-6, Ki-67 and Bcl-XL was performed for 101 cases of resected HCC, and correlations between pSTAT3 staining and clinicopathological findings were analyzed. In HCC cell lines (PLC/PRF/5 and Huh7), cell proliferation and migration by IL-6 stimulation and S3I-201 (STAT3 inhibitor) treatment were analyzed. Results: In HCC specimens, the pSTAT3-positive group showed high levels of α-fetoprotein (p = 0.0276), large tumor size (p = 0.0092), frequent intrahepatic metastasis (p = 0.0214), high Ki-67 (p = 0.0002) and Bcl-XL (p = 0.0001), poor prognosis (p = 0.0234), and high recurrence rate (p = 0.0003). CD163-positive cells were frequently observed in the pSTAT3-positive group (p = 0.0013). In two HCC cell lines, IL-6 stimulation promoted cell proliferation and migration via the STAT3 phosphorylation, and S3I-201 inhibited this activation. Conclusions: STAT3 activation was correlated with aggressive behavior of HCC and may be mediated via tumor-associated macrophage. We expect that STAT3 signaling and tumor-associated macrophages can be attractive therapeutic targets in HCC patients.</description><subject>Cancer therapies</subject><subject>Carcinoma, Hepatocellular - immunology</subject><subject>Carcinoma, Hepatocellular - metabolism</subject><subject>Carcinoma, Hepatocellular - pathology</subject><subject>Disease Progression</subject><subject>Female</subject><subject>Humans</subject><subject>Immunoblotting</subject><subject>Immunohistochemistry</subject><subject>Liver cancer</subject><subject>Liver Neoplasms - immunology</subject><subject>Liver Neoplasms - metabolism</subject><subject>Liver Neoplasms - pathology</subject><subject>Macrophages - immunology</subject><subject>Macrophages - metabolism</subject><subject>Male</subject><subject>Metastasis</subject><subject>Middle Aged</subject><subject>Original Paper</subject><subject>Pathology</subject><subject>Signal Transduction - physiology</subject><subject>STAT3 Transcription Factor - metabolism</subject><subject>Tumors</subject><issn>1015-2008</issn><issn>1423-0291</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpd0M1LwzAYBvAgis6Pg3eRgBc9VJMmTdvjGOoERcF5Lm_StGa2zUxawf_e1M0dPCWB3_uS50HolJJrSpP8hhDCuKC52EETymMWkTinu-FOaBLFhGQH6ND7ZWAZEWQfHcSMCc6yfIKqxdBaF029t8pAr0v8BMrZ1TvUGr8429pee_yLxmfttPfGdvjLAH5dTBcMv5q6g8Z0NTYdnusV9FbpphkacHgGTpnOtnCM9ipovD7ZnEfo7e52MZtHj8_3D7PpY6S44H0kE6qlikvF0qTKCCNElyGZyKDilaSEpJKCEjlPQYuU8qyMpVJcgsxlkoZUR-hyvXfl7OegfV-0xo_fgU7bwReUxSzNheBJoBf_6NIOLkQZFc8oSwQTQV2tVSjFe6erYuVMC-67oKQYyy-25Qd7vtk4yFaXW_nXdgBna_ABrtZuCzbzPwMEh2U</recordid><startdate>20130101</startdate><enddate>20130101</enddate><creator>Mano, Yohei</creator><creator>Aishima, Shinichi</creator><creator>Fujita, Nobuhiro</creator><creator>Tanaka, Yuki</creator><creator>Kubo, Yuichiro</creator><creator>Motomura, Takashi</creator><creator>Taketomi, Akinobu</creator><creator>Shirabe, Ken</creator><creator>Maehara, Yoshihiko</creator><creator>Oda, Yoshinao</creator><general>S. 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immunology</topic><topic>Carcinoma, Hepatocellular - metabolism</topic><topic>Carcinoma, Hepatocellular - pathology</topic><topic>Disease Progression</topic><topic>Female</topic><topic>Humans</topic><topic>Immunoblotting</topic><topic>Immunohistochemistry</topic><topic>Liver cancer</topic><topic>Liver Neoplasms - immunology</topic><topic>Liver Neoplasms - metabolism</topic><topic>Liver Neoplasms - pathology</topic><topic>Macrophages - immunology</topic><topic>Macrophages - metabolism</topic><topic>Male</topic><topic>Metastasis</topic><topic>Middle Aged</topic><topic>Original Paper</topic><topic>Pathology</topic><topic>Signal Transduction - physiology</topic><topic>STAT3 Transcription Factor - metabolism</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mano, Yohei</creatorcontrib><creatorcontrib>Aishima, Shinichi</creatorcontrib><creatorcontrib>Fujita, Nobuhiro</creatorcontrib><creatorcontrib>Tanaka, Yuki</creatorcontrib><creatorcontrib>Kubo, Yuichiro</creatorcontrib><creatorcontrib>Motomura, Takashi</creatorcontrib><creatorcontrib>Taketomi, Akinobu</creatorcontrib><creatorcontrib>Shirabe, Ken</creatorcontrib><creatorcontrib>Maehara, Yoshihiko</creatorcontrib><creatorcontrib>Oda, Yoshinao</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>ProQuest Nursing and Allied Health Journals</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database (Proquest)</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)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Earth, Atmospheric & Aquatic Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</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>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Science Journals</collection><collection>ProQuest Biological Science Journals</collection><collection>Nursing & Allied Health Premium</collection><collection>Earth, Atmospheric & Aquatic 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 Basic</collection><collection>SIRS Editorial</collection><collection>MEDLINE - Academic</collection><jtitle>Pathobiology (Basel)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mano, Yohei</au><au>Aishima, Shinichi</au><au>Fujita, Nobuhiro</au><au>Tanaka, Yuki</au><au>Kubo, Yuichiro</au><au>Motomura, Takashi</au><au>Taketomi, Akinobu</au><au>Shirabe, Ken</au><au>Maehara, Yoshihiko</au><au>Oda, Yoshinao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tumor-Associated Macrophage Promotes Tumor Progression via STAT3 Signaling in Hepatocellular Carcinoma</atitle><jtitle>Pathobiology (Basel)</jtitle><addtitle>Pathobiology</addtitle><date>2013-01-01</date><risdate>2013</risdate><volume>80</volume><issue>3</issue><spage>146</spage><epage>154</epage><pages>146-154</pages><issn>1015-2008</issn><eissn>1423-0291</eissn><coden>PATHEF</coden><abstract>Objective: Signal transducer and activator of transcription 3 (STAT3) is activated in hepatocellular carcinoma (HCC), and tumor-associated macrophage plays an important role in tumor progression. Therefore, we examined STAT3 activation, cytokine expression and infiltration of tumor-associated macrophages in resected HCCs as well as the alteration of cell growth and migration by cytokine stimulation in HCC cell lines. Methods: Immunohistochemical staining of phosphorylated STAT3 (pSTAT3), CD163, interleukin (IL)-6, Ki-67 and Bcl-XL was performed for 101 cases of resected HCC, and correlations between pSTAT3 staining and clinicopathological findings were analyzed. In HCC cell lines (PLC/PRF/5 and Huh7), cell proliferation and migration by IL-6 stimulation and S3I-201 (STAT3 inhibitor) treatment were analyzed. Results: In HCC specimens, the pSTAT3-positive group showed high levels of α-fetoprotein (p = 0.0276), large tumor size (p = 0.0092), frequent intrahepatic metastasis (p = 0.0214), high Ki-67 (p = 0.0002) and Bcl-XL (p = 0.0001), poor prognosis (p = 0.0234), and high recurrence rate (p = 0.0003). CD163-positive cells were frequently observed in the pSTAT3-positive group (p = 0.0013). In two HCC cell lines, IL-6 stimulation promoted cell proliferation and migration via the STAT3 phosphorylation, and S3I-201 inhibited this activation. Conclusions: STAT3 activation was correlated with aggressive behavior of HCC and may be mediated via tumor-associated macrophage. We expect that STAT3 signaling and tumor-associated macrophages can be attractive therapeutic targets in HCC patients.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>23364389</pmid><doi>10.1159/000346196</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Cancer therapies Carcinoma, Hepatocellular - immunology Carcinoma, Hepatocellular - metabolism Carcinoma, Hepatocellular - pathology Disease Progression Female Humans Immunoblotting Immunohistochemistry Liver cancer Liver Neoplasms - immunology Liver Neoplasms - metabolism Liver Neoplasms - pathology Macrophages - immunology Macrophages - metabolism Male Metastasis Middle Aged Original Paper Pathology Signal Transduction - physiology STAT3 Transcription Factor - metabolism Tumors |
| title | Tumor-Associated Macrophage Promotes Tumor Progression via STAT3 Signaling in Hepatocellular Carcinoma |
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