Tip60 Suppresses Cholangiocarcinoma Proliferation and Metastasis via PI3k-AKT
Background/Aims: Aberrant expression of Tip60 is associated with progression in many cancers. However, the role of Tip60 in cancer progression remains contradictory. The aim of this study was to investigate the clinical significance, biological functions and underlying mechanisms of Tip60 deregulati...
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| Veröffentlicht in: | Cellular Physiology and Biochemistry 2018-10, Vol.50 (2), p.612-628 |
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| creator | Zhang, Yaodong Ji, Guwei Han, Sheng Shao, Zicheng Lu, Zefa Huo, Liqun Zhang, Jiawei Yang, Renjie Feng, Qinchao Shen, Hao Wang, Hongwei Li, Xiangcheng |
| description | Background/Aims: Aberrant expression of Tip60 is associated with progression in many cancers. However, the role of Tip60 in cancer progression remains contradictory. The aim of this study was to investigate the clinical significance, biological functions and underlying mechanisms of Tip60 deregulation in cholangiocarcinoma (CCA) for the first time. Methods: Quantitative real-time PCR (QRT-PCR), western blotting and immunohistochemistry staining (IHC) were carried out to measure Tip60 expression in CCA tissues and cell lines. Kaplan–Meier analysis and the log-rank test were used for survival analysis. In vitro, cell proliferation was evaluated by flow cytometry and CCK-8, colony formation, and EDU assays. Migration/ invasion was evaluated by trans-well assays. Phosphokinase array was used to confirm the dominant signal regulated by Tip60. Tumor growth and metastasis were demonstrated in vivo using a mouse model. Results: Tip60 was notably downregulated in CCA tissues, which was associated with greater tumor size, venous invasion, and TNM stage. Down-regulation of Tip60 was associated with tumor progression and poorer survival in CCA patients. In vitro and in vivo studies demonstrated that Tip60 suppressed growth and metastasis throughout the progression of CCA. We further identified the PI3K/AKT pathway as a dominant signal of Tip60 and suggested that Tip60 regulated CCA cell proliferation and metastasis via PT3K-AKT pathway. Pearson analysis revealed that PTEN was positively correlated with the Tip60 level in CCA tissues. Conclusion: Tip60, as a tumor suppressor in CCA via the PI3K/AKT pathway, might be a promising therapeutic target or prognostic marker for CCA. |
| doi_str_mv | 10.1159/000494183 |
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However, the role of Tip60 in cancer progression remains contradictory. The aim of this study was to investigate the clinical significance, biological functions and underlying mechanisms of Tip60 deregulation in cholangiocarcinoma (CCA) for the first time. Methods: Quantitative real-time PCR (QRT-PCR), western blotting and immunohistochemistry staining (IHC) were carried out to measure Tip60 expression in CCA tissues and cell lines. Kaplan–Meier analysis and the log-rank test were used for survival analysis. In vitro, cell proliferation was evaluated by flow cytometry and CCK-8, colony formation, and EDU assays. Migration/ invasion was evaluated by trans-well assays. Phosphokinase array was used to confirm the dominant signal regulated by Tip60. Tumor growth and metastasis were demonstrated in vivo using a mouse model. Results: Tip60 was notably downregulated in CCA tissues, which was associated with greater tumor size, venous invasion, and TNM stage. Down-regulation of Tip60 was associated with tumor progression and poorer survival in CCA patients. In vitro and in vivo studies demonstrated that Tip60 suppressed growth and metastasis throughout the progression of CCA. We further identified the PI3K/AKT pathway as a dominant signal of Tip60 and suggested that Tip60 regulated CCA cell proliferation and metastasis via PT3K-AKT pathway. Pearson analysis revealed that PTEN was positively correlated with the Tip60 level in CCA tissues. Conclusion: Tip60, as a tumor suppressor in CCA via the PI3K/AKT pathway, might be a promising therapeutic target or prognostic marker for CCA.</description><identifier>ISSN: 1015-8987</identifier><identifier>EISSN: 1421-9778</identifier><identifier>DOI: 10.1159/000494183</identifier><identifier>PMID: 30308494</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Animals ; Bile Duct Neoplasms - metabolism ; Bile Duct Neoplasms - mortality ; Bile Duct Neoplasms - pathology ; Care and treatment ; Cell adhesion & migration ; Cell cycle ; Cell Line, Tumor ; Cell Proliferation ; Cholangiocarcinoma ; Cholangiocarcinoma - metabolism ; Cholangiocarcinoma - mortality ; Cholangiocarcinoma - pathology ; Development and progression ; DNA repair ; Female ; Genetic aspects ; Health aspects ; Humans ; Kinases ; Lysine Acetyltransferase 5 - antagonists & inhibitors ; Lysine Acetyltransferase 5 - genetics ; Lysine Acetyltransferase 5 - metabolism ; Male ; Medical prognosis ; Metastasis ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Middle Aged ; Neoplasm Metastasis ; Original Paper ; Phosphatidylinositol 3-Kinases - metabolism ; Physiological aspects ; Prevention ; Proliferation ; Prostate cancer ; Proteins ; Proto-Oncogene Proteins c-akt - metabolism ; PTEN Phosphohydrolase - metabolism ; RNA Interference ; RNA, Small Interfering - metabolism ; Signal Transduction ; Software ; Tip60 ; Tumor suppressor genes</subject><ispartof>Cellular Physiology and Biochemistry, 2018-10, Vol.50 (2), p.612-628</ispartof><rights>2018 The Author(s). Published by S. Karger AG, Basel</rights><rights>2018 The Author(s). Published by S. Karger AG, Basel.</rights><rights>COPYRIGHT 2018 S. Karger AG</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c530t-42087b9183a2f0bca17f66b930f7072f3f402eda974ac87a90858afbda4596983</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,864,2102,27635,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30308494$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Yaodong</creatorcontrib><creatorcontrib>Ji, Guwei</creatorcontrib><creatorcontrib>Han, Sheng</creatorcontrib><creatorcontrib>Shao, Zicheng</creatorcontrib><creatorcontrib>Lu, Zefa</creatorcontrib><creatorcontrib>Huo, Liqun</creatorcontrib><creatorcontrib>Zhang, Jiawei</creatorcontrib><creatorcontrib>Yang, Renjie</creatorcontrib><creatorcontrib>Feng, Qinchao</creatorcontrib><creatorcontrib>Shen, Hao</creatorcontrib><creatorcontrib>Wang, Hongwei</creatorcontrib><creatorcontrib>Li, Xiangcheng</creatorcontrib><title>Tip60 Suppresses Cholangiocarcinoma Proliferation and Metastasis via PI3k-AKT</title><title>Cellular Physiology and Biochemistry</title><addtitle>Cell Physiol Biochem</addtitle><description>Background/Aims: Aberrant expression of Tip60 is associated with progression in many cancers. However, the role of Tip60 in cancer progression remains contradictory. The aim of this study was to investigate the clinical significance, biological functions and underlying mechanisms of Tip60 deregulation in cholangiocarcinoma (CCA) for the first time. Methods: Quantitative real-time PCR (QRT-PCR), western blotting and immunohistochemistry staining (IHC) were carried out to measure Tip60 expression in CCA tissues and cell lines. Kaplan–Meier analysis and the log-rank test were used for survival analysis. In vitro, cell proliferation was evaluated by flow cytometry and CCK-8, colony formation, and EDU assays. Migration/ invasion was evaluated by trans-well assays. Phosphokinase array was used to confirm the dominant signal regulated by Tip60. Tumor growth and metastasis were demonstrated in vivo using a mouse model. Results: Tip60 was notably downregulated in CCA tissues, which was associated with greater tumor size, venous invasion, and TNM stage. Down-regulation of Tip60 was associated with tumor progression and poorer survival in CCA patients. In vitro and in vivo studies demonstrated that Tip60 suppressed growth and metastasis throughout the progression of CCA. We further identified the PI3K/AKT pathway as a dominant signal of Tip60 and suggested that Tip60 regulated CCA cell proliferation and metastasis via PT3K-AKT pathway. Pearson analysis revealed that PTEN was positively correlated with the Tip60 level in CCA tissues. Conclusion: Tip60, as a tumor suppressor in CCA via the PI3K/AKT pathway, might be a promising therapeutic target or prognostic marker for CCA.</description><subject>Animals</subject><subject>Bile Duct Neoplasms - metabolism</subject><subject>Bile Duct Neoplasms - mortality</subject><subject>Bile Duct Neoplasms - pathology</subject><subject>Care and treatment</subject><subject>Cell adhesion & migration</subject><subject>Cell cycle</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Cholangiocarcinoma</subject><subject>Cholangiocarcinoma - metabolism</subject><subject>Cholangiocarcinoma - mortality</subject><subject>Cholangiocarcinoma - pathology</subject><subject>Development and progression</subject><subject>DNA repair</subject><subject>Female</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Kinases</subject><subject>Lysine Acetyltransferase 5 - antagonists & inhibitors</subject><subject>Lysine Acetyltransferase 5 - genetics</subject><subject>Lysine Acetyltransferase 5 - metabolism</subject><subject>Male</subject><subject>Medical prognosis</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Middle Aged</subject><subject>Neoplasm Metastasis</subject><subject>Original Paper</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Physiological aspects</subject><subject>Prevention</subject><subject>Proliferation</subject><subject>Prostate cancer</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>PTEN Phosphohydrolase - metabolism</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering - metabolism</subject><subject>Signal Transduction</subject><subject>Software</subject><subject>Tip60</subject><subject>Tumor suppressor genes</subject><issn>1015-8987</issn><issn>1421-9778</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>M--</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DOA</sourceid><recordid>eNptkU1v1DAQhiMEoqVw4I5QpF7gkDKOHX8clxWFFa2oxHK2Jo69eJvEqZ1F4t_XJWUPCNmS7fHzvp7xFMVrAheENOoDADDFiKRPilPCalIpIeTTvAfSVFJJcVK8SGkP-ShU_bw4oUBBZslpcb31E4fy-2Gaok3JpnL9M_Q47nwwGI0fw4DlTQy9dzbi7MNY4tiV13bGlKdP5S-fgQ29rVZfty-LZw77ZF89rmfFj8tP2_WX6urb5816dVWZhsJcsRqkaFVOGGsHrUEiHOetouAEiNpRx6C2HSrB0EiBCmQj0bUdskZxJelZsVl8u4B7PUU_YPytA3r9JxDiTmOcvemtFmg4OMc4kw1rLEXb8hY4yJo7TqDNXu8WrymGu4NNsx58MrbPn2DDIemaEKVqTiXN6Pk_6D4c4pgr1TUFIhVj5IG6WKgd5vf96MIc0eTR2cGbMFrnc3zFqWgoodBkwftFYGJIKVp3rIiAfmiwPjY4s28fUzi0g-2O5N-OZuDNAtxi3Nl4BI768_9er28-LoSeOkfvARAesTo</recordid><startdate>20181001</startdate><enddate>20181001</enddate><creator>Zhang, Yaodong</creator><creator>Ji, Guwei</creator><creator>Han, Sheng</creator><creator>Shao, Zicheng</creator><creator>Lu, Zefa</creator><creator>Huo, Liqun</creator><creator>Zhang, Jiawei</creator><creator>Yang, Renjie</creator><creator>Feng, Qinchao</creator><creator>Shen, Hao</creator><creator>Wang, Hongwei</creator><creator>Li, Xiangcheng</creator><general>S. Karger AG</general><general>Cell Physiol Biochem Press GmbH & Co KG</general><scope>M--</scope><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>IAO</scope><scope>3V.</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>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</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><scope>DOA</scope></search><sort><creationdate>20181001</creationdate><title>Tip60 Suppresses Cholangiocarcinoma Proliferation and Metastasis via PI3k-AKT</title><author>Zhang, Yaodong ; Ji, Guwei ; Han, Sheng ; Shao, Zicheng ; Lu, Zefa ; Huo, Liqun ; Zhang, Jiawei ; Yang, Renjie ; Feng, Qinchao ; Shen, Hao ; Wang, Hongwei ; Li, Xiangcheng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c530t-42087b9183a2f0bca17f66b930f7072f3f402eda974ac87a90858afbda4596983</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animals</topic><topic>Bile Duct Neoplasms - metabolism</topic><topic>Bile Duct Neoplasms - mortality</topic><topic>Bile Duct Neoplasms - pathology</topic><topic>Care and treatment</topic><topic>Cell adhesion & migration</topic><topic>Cell cycle</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Cholangiocarcinoma</topic><topic>Cholangiocarcinoma - metabolism</topic><topic>Cholangiocarcinoma - mortality</topic><topic>Cholangiocarcinoma - pathology</topic><topic>Development and progression</topic><topic>DNA repair</topic><topic>Female</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Kinases</topic><topic>Lysine Acetyltransferase 5 - antagonists & inhibitors</topic><topic>Lysine Acetyltransferase 5 - genetics</topic><topic>Lysine Acetyltransferase 5 - metabolism</topic><topic>Male</topic><topic>Medical prognosis</topic><topic>Metastasis</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>Middle Aged</topic><topic>Neoplasm Metastasis</topic><topic>Original Paper</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Physiological aspects</topic><topic>Prevention</topic><topic>Proliferation</topic><topic>Prostate cancer</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>PTEN Phosphohydrolase - metabolism</topic><topic>RNA Interference</topic><topic>RNA, Small Interfering - metabolism</topic><topic>Signal Transduction</topic><topic>Software</topic><topic>Tip60</topic><topic>Tumor suppressor genes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Yaodong</creatorcontrib><creatorcontrib>Ji, Guwei</creatorcontrib><creatorcontrib>Han, Sheng</creatorcontrib><creatorcontrib>Shao, Zicheng</creatorcontrib><creatorcontrib>Lu, Zefa</creatorcontrib><creatorcontrib>Huo, Liqun</creatorcontrib><creatorcontrib>Zhang, Jiawei</creatorcontrib><creatorcontrib>Yang, Renjie</creatorcontrib><creatorcontrib>Feng, Qinchao</creatorcontrib><creatorcontrib>Shen, Hao</creatorcontrib><creatorcontrib>Wang, Hongwei</creatorcontrib><creatorcontrib>Li, Xiangcheng</creatorcontrib><collection>Karger Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale Academic OneFile</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>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>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><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Cellular Physiology and Biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Yaodong</au><au>Ji, Guwei</au><au>Han, Sheng</au><au>Shao, Zicheng</au><au>Lu, Zefa</au><au>Huo, Liqun</au><au>Zhang, Jiawei</au><au>Yang, Renjie</au><au>Feng, Qinchao</au><au>Shen, Hao</au><au>Wang, Hongwei</au><au>Li, Xiangcheng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tip60 Suppresses Cholangiocarcinoma Proliferation and Metastasis via PI3k-AKT</atitle><jtitle>Cellular Physiology and Biochemistry</jtitle><addtitle>Cell Physiol Biochem</addtitle><date>2018-10-01</date><risdate>2018</risdate><volume>50</volume><issue>2</issue><spage>612</spage><epage>628</epage><pages>612-628</pages><issn>1015-8987</issn><eissn>1421-9778</eissn><abstract>Background/Aims: Aberrant expression of Tip60 is associated with progression in many cancers. However, the role of Tip60 in cancer progression remains contradictory. The aim of this study was to investigate the clinical significance, biological functions and underlying mechanisms of Tip60 deregulation in cholangiocarcinoma (CCA) for the first time. Methods: Quantitative real-time PCR (QRT-PCR), western blotting and immunohistochemistry staining (IHC) were carried out to measure Tip60 expression in CCA tissues and cell lines. Kaplan–Meier analysis and the log-rank test were used for survival analysis. In vitro, cell proliferation was evaluated by flow cytometry and CCK-8, colony formation, and EDU assays. Migration/ invasion was evaluated by trans-well assays. Phosphokinase array was used to confirm the dominant signal regulated by Tip60. Tumor growth and metastasis were demonstrated in vivo using a mouse model. Results: Tip60 was notably downregulated in CCA tissues, which was associated with greater tumor size, venous invasion, and TNM stage. Down-regulation of Tip60 was associated with tumor progression and poorer survival in CCA patients. In vitro and in vivo studies demonstrated that Tip60 suppressed growth and metastasis throughout the progression of CCA. We further identified the PI3K/AKT pathway as a dominant signal of Tip60 and suggested that Tip60 regulated CCA cell proliferation and metastasis via PT3K-AKT pathway. Pearson analysis revealed that PTEN was positively correlated with the Tip60 level in CCA tissues. Conclusion: Tip60, as a tumor suppressor in CCA via the PI3K/AKT pathway, might be a promising therapeutic target or prognostic marker for CCA.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>30308494</pmid><doi>10.1159/000494183</doi><tpages>17</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Bile Duct Neoplasms - metabolism Bile Duct Neoplasms - mortality Bile Duct Neoplasms - pathology Care and treatment Cell adhesion & migration Cell cycle Cell Line, Tumor Cell Proliferation Cholangiocarcinoma Cholangiocarcinoma - metabolism Cholangiocarcinoma - mortality Cholangiocarcinoma - pathology Development and progression DNA repair Female Genetic aspects Health aspects Humans Kinases Lysine Acetyltransferase 5 - antagonists & inhibitors Lysine Acetyltransferase 5 - genetics Lysine Acetyltransferase 5 - metabolism Male Medical prognosis Metastasis Mice Mice, Inbred BALB C Mice, Nude Middle Aged Neoplasm Metastasis Original Paper Phosphatidylinositol 3-Kinases - metabolism Physiological aspects Prevention Proliferation Prostate cancer Proteins Proto-Oncogene Proteins c-akt - metabolism PTEN Phosphohydrolase - metabolism RNA Interference RNA, Small Interfering - metabolism Signal Transduction Software Tip60 Tumor suppressor genes |
| title | Tip60 Suppresses Cholangiocarcinoma Proliferation and Metastasis via PI3k-AKT |
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