Actin‐like 6A predicts poor prognosis of hepatocellular carcinoma and promotes metastasis and epithelial‐mesenchymal transition
Hepatocellular carcinoma (HCC) is one of the most lethal cancers worldwide because of metastasis. Epithelial‐mesenchymal transition (EMT) is widely considered to be crucial to the invasion‐metastasis cascade during cancer progression. Actin‐like 6A (ACTL6A) is initially verified important for cell p...
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| Veröffentlicht in: | Hepatology (Baltimore, Md.) Md.), 2016-04, Vol.63 (4), p.1256-1271 |
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| container_title | Hepatology (Baltimore, Md.) |
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| creator | Xiao, Shuai Chang, Rui‐Min Yang, Ming‐Yang Lei, Xiong Liu, Xiao Gao, Wen‐Bin Xiao, Jing‐Lei Yang, Lian‐Yue |
| description | Hepatocellular carcinoma (HCC) is one of the most lethal cancers worldwide because of metastasis. Epithelial‐mesenchymal transition (EMT) is widely considered to be crucial to the invasion‐metastasis cascade during cancer progression. Actin‐like 6A (ACTL6A) is initially verified important for cell proliferation, differentiation, and migration. In this study, we find that ACTL6A plays an essential role in metastasis and EMT of HCC. ACTL6A expression is up‐regulated in HCC cells and tissues. A high level of ACTL6A in HCCs is correlated with aggressive clinicopathological features and is an independent poor prognostic factor for overall and disease‐free survival of HCC patients. Ectopic expression of ACTL6A markedly promotes HCC cells migration, invasion, as well as EMT in vitro and promotes tumor growth and metastasis in the mouse xenograft model. Opposite results are observed when ACTL6A is knocked down. Mechanistically, ACTL6A promotes metastasis and EMT through activating Notch signaling. ACTL6A knockdown has the equal blockage effect as the Notch signaling inhibitor, N‐[N‐(3,5‐difluorophenacetyl)‐L‐alanyl]‐S‐phenylglycine t‐butylester, in HCC cells. Further studies indicate that ACTL6A might manipulate SRY (sex determining region Y)‐box 2 (SOX2) expression and then activate Notch1 signaling. Conclusions: ACTL6A promotes metastasis and EMT by SOX2/Notch1 signaling, indicating a prognostic biomarker candidate and a potential therapeutic target for HCC. (Hepatology 2016;63:1256–1271) |
| doi_str_mv | 10.1002/hep.28417 |
| format | Article |
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Epithelial‐mesenchymal transition (EMT) is widely considered to be crucial to the invasion‐metastasis cascade during cancer progression. Actin‐like 6A (ACTL6A) is initially verified important for cell proliferation, differentiation, and migration. In this study, we find that ACTL6A plays an essential role in metastasis and EMT of HCC. ACTL6A expression is up‐regulated in HCC cells and tissues. A high level of ACTL6A in HCCs is correlated with aggressive clinicopathological features and is an independent poor prognostic factor for overall and disease‐free survival of HCC patients. Ectopic expression of ACTL6A markedly promotes HCC cells migration, invasion, as well as EMT in vitro and promotes tumor growth and metastasis in the mouse xenograft model. Opposite results are observed when ACTL6A is knocked down. Mechanistically, ACTL6A promotes metastasis and EMT through activating Notch signaling. ACTL6A knockdown has the equal blockage effect as the Notch signaling inhibitor, N‐[N‐(3,5‐difluorophenacetyl)‐L‐alanyl]‐S‐phenylglycine t‐butylester, in HCC cells. Further studies indicate that ACTL6A might manipulate SRY (sex determining region Y)‐box 2 (SOX2) expression and then activate Notch1 signaling. Conclusions: ACTL6A promotes metastasis and EMT by SOX2/Notch1 signaling, indicating a prognostic biomarker candidate and a potential therapeutic target for HCC. (Hepatology 2016;63:1256–1271)</description><identifier>ISSN: 0270-9139</identifier><identifier>EISSN: 1527-3350</identifier><identifier>DOI: 10.1002/hep.28417</identifier><identifier>PMID: 26698646</identifier><identifier>CODEN: HPTLD9</identifier><language>eng</language><publisher>United States: Wolters Kluwer Health, Inc</publisher><subject>Actin ; Actins - genetics ; Adult ; Aged ; Analysis of Variance ; Animals ; Biopsy, Needle ; Carcinoma, Hepatocellular - genetics ; Carcinoma, Hepatocellular - mortality ; Carcinoma, Hepatocellular - pathology ; Cell adhesion & migration ; Cell migration ; Cell proliferation ; Chromosomal Proteins, Non-Histone - genetics ; Disease Models, Animal ; DNA-Binding Proteins - genetics ; Ectopic expression ; Epithelial-Mesenchymal Transition - genetics ; Female ; Gene Expression Regulation, Neoplastic ; Hepatobiliary Malignancies ; Hepatocellular carcinoma ; Hepatology ; Humans ; Immunohistochemistry ; Liver cancer ; Liver Neoplasms - genetics ; Liver Neoplasms - mortality ; Liver Neoplasms - pathology ; Male ; Medical prognosis ; Mesenchyme ; Metastases ; Metastasis ; Mice ; Middle Aged ; Multivariate Analysis ; Neoplasm Invasiveness - pathology ; Neoplasm Metastasis - genetics ; Notch1 protein ; Phenylglycine ; Predictive Value of Tests ; Prognosis ; Random Allocation ; Survival Analysis ; Transcriptional Activation ; Tumor Cells, Cultured ; Up-Regulation ; Xenografts</subject><ispartof>Hepatology (Baltimore, Md.), 2016-04, Vol.63 (4), p.1256-1271</ispartof><rights>2015 The Authors. H published by Wiley Periodicals, Inc., on behalf of American Association for the Study of Liver Diseases.</rights><rights>2015 The Authors. Hepatology published by Wiley Periodicals, Inc., on behalf of American Association for the Study of Liver Diseases.</rights><rights>2016 by the American Association for the Study of Liver Diseases</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5707-ea03aed1bbe787c3af05ba4a9103695be71a3aab636f51c83e325aca891546a23</citedby><cites>FETCH-LOGICAL-c5707-ea03aed1bbe787c3af05ba4a9103695be71a3aab636f51c83e325aca891546a23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fhep.28417$$EPDF$$P50$$Gwiley$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fhep.28417$$EHTML$$P50$$Gwiley$$Hfree_for_read</linktohtml><link.rule.ids>230,314,780,784,885,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26698646$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xiao, Shuai</creatorcontrib><creatorcontrib>Chang, Rui‐Min</creatorcontrib><creatorcontrib>Yang, Ming‐Yang</creatorcontrib><creatorcontrib>Lei, Xiong</creatorcontrib><creatorcontrib>Liu, Xiao</creatorcontrib><creatorcontrib>Gao, Wen‐Bin</creatorcontrib><creatorcontrib>Xiao, Jing‐Lei</creatorcontrib><creatorcontrib>Yang, Lian‐Yue</creatorcontrib><title>Actin‐like 6A predicts poor prognosis of hepatocellular carcinoma and promotes metastasis and epithelial‐mesenchymal transition</title><title>Hepatology (Baltimore, Md.)</title><addtitle>Hepatology</addtitle><description>Hepatocellular carcinoma (HCC) is one of the most lethal cancers worldwide because of metastasis. Epithelial‐mesenchymal transition (EMT) is widely considered to be crucial to the invasion‐metastasis cascade during cancer progression. Actin‐like 6A (ACTL6A) is initially verified important for cell proliferation, differentiation, and migration. In this study, we find that ACTL6A plays an essential role in metastasis and EMT of HCC. ACTL6A expression is up‐regulated in HCC cells and tissues. A high level of ACTL6A in HCCs is correlated with aggressive clinicopathological features and is an independent poor prognostic factor for overall and disease‐free survival of HCC patients. Ectopic expression of ACTL6A markedly promotes HCC cells migration, invasion, as well as EMT in vitro and promotes tumor growth and metastasis in the mouse xenograft model. Opposite results are observed when ACTL6A is knocked down. Mechanistically, ACTL6A promotes metastasis and EMT through activating Notch signaling. ACTL6A knockdown has the equal blockage effect as the Notch signaling inhibitor, N‐[N‐(3,5‐difluorophenacetyl)‐L‐alanyl]‐S‐phenylglycine t‐butylester, in HCC cells. Further studies indicate that ACTL6A might manipulate SRY (sex determining region Y)‐box 2 (SOX2) expression and then activate Notch1 signaling. Conclusions: ACTL6A promotes metastasis and EMT by SOX2/Notch1 signaling, indicating a prognostic biomarker candidate and a potential therapeutic target for HCC. (Hepatology 2016;63:1256–1271)</description><subject>Actin</subject><subject>Actins - genetics</subject><subject>Adult</subject><subject>Aged</subject><subject>Analysis of Variance</subject><subject>Animals</subject><subject>Biopsy, Needle</subject><subject>Carcinoma, Hepatocellular - genetics</subject><subject>Carcinoma, Hepatocellular - mortality</subject><subject>Carcinoma, Hepatocellular - pathology</subject><subject>Cell adhesion & migration</subject><subject>Cell migration</subject><subject>Cell proliferation</subject><subject>Chromosomal Proteins, Non-Histone - genetics</subject><subject>Disease Models, Animal</subject><subject>DNA-Binding Proteins - genetics</subject><subject>Ectopic expression</subject><subject>Epithelial-Mesenchymal Transition - genetics</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Hepatobiliary Malignancies</subject><subject>Hepatocellular carcinoma</subject><subject>Hepatology</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Liver cancer</subject><subject>Liver Neoplasms - genetics</subject><subject>Liver Neoplasms - mortality</subject><subject>Liver Neoplasms - pathology</subject><subject>Male</subject><subject>Medical prognosis</subject><subject>Mesenchyme</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Middle Aged</subject><subject>Multivariate Analysis</subject><subject>Neoplasm Invasiveness - pathology</subject><subject>Neoplasm Metastasis - genetics</subject><subject>Notch1 protein</subject><subject>Phenylglycine</subject><subject>Predictive Value of Tests</subject><subject>Prognosis</subject><subject>Random Allocation</subject><subject>Survival Analysis</subject><subject>Transcriptional Activation</subject><subject>Tumor Cells, Cultured</subject><subject>Up-Regulation</subject><subject>Xenografts</subject><issn>0270-9139</issn><issn>1527-3350</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>EIF</sourceid><recordid>eNqNkt9qFTEQxoMo9li98AVkwRu92DZ_dpPdG-FQWisU9EKvw2zObE9qNlmT3cq5E3yBPqNPYtZTiwqKEAiZ_PJ9k5kh5CmjR4xSfrzF8Yg3FVP3yIrVXJVC1PQ-WVGuaNky0R6QRyldUUrbijcPyQGXsm1kJVfk69pM1n_7cuPsRyzkuhgjbqyZUjGGEPMpXPqQbCpCX2QbmIJB52YHsTAQjfVhgAL8ZiGHMGEqBpwg5ZXfLHEc7bRFZ8FlkwETerPdDeCKKYJPdrLBPyYPenAJn9zuh-TD2en7k_Py4u3rNyfri9LUiqoSgQrADes6VI0yAnpad1BBy6iQbZ2jDARAJ4Xsa2YagYLXYKBpWV1J4OKQvNrrjnM34Magzzk4PUY7QNzpAFb_fuPtVl-Ga101olJcZYEXtwIxfJoxTXqwaakHeAxz0kw1tKZcNv-DKklboVib0ed_oFdhjj5XQrOWKkEFU9U_KaXq3FdVLbYv95SJIaWI_d3vGNXLrOjcRP1jVjL77Ndy3JE_hyMDx3vgs3W4-7uSPj99t5f8Dme1zSo</recordid><startdate>201604</startdate><enddate>201604</enddate><creator>Xiao, Shuai</creator><creator>Chang, Rui‐Min</creator><creator>Yang, Ming‐Yang</creator><creator>Lei, Xiong</creator><creator>Liu, Xiao</creator><creator>Gao, Wen‐Bin</creator><creator>Xiao, Jing‐Lei</creator><creator>Yang, Lian‐Yue</creator><general>Wolters Kluwer Health, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</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>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201604</creationdate><title>Actin‐like 6A predicts poor prognosis of hepatocellular carcinoma and promotes metastasis and epithelial‐mesenchymal transition</title><author>Xiao, Shuai ; Chang, Rui‐Min ; Yang, Ming‐Yang ; Lei, Xiong ; Liu, Xiao ; Gao, Wen‐Bin ; Xiao, Jing‐Lei ; Yang, Lian‐Yue</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5707-ea03aed1bbe787c3af05ba4a9103695be71a3aab636f51c83e325aca891546a23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Actin</topic><topic>Actins - genetics</topic><topic>Adult</topic><topic>Aged</topic><topic>Analysis of Variance</topic><topic>Animals</topic><topic>Biopsy, Needle</topic><topic>Carcinoma, Hepatocellular - genetics</topic><topic>Carcinoma, Hepatocellular - mortality</topic><topic>Carcinoma, Hepatocellular - pathology</topic><topic>Cell adhesion & migration</topic><topic>Cell migration</topic><topic>Cell proliferation</topic><topic>Chromosomal Proteins, Non-Histone - genetics</topic><topic>Disease Models, Animal</topic><topic>DNA-Binding Proteins - genetics</topic><topic>Ectopic expression</topic><topic>Epithelial-Mesenchymal Transition - genetics</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Hepatobiliary Malignancies</topic><topic>Hepatocellular carcinoma</topic><topic>Hepatology</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Liver cancer</topic><topic>Liver Neoplasms - genetics</topic><topic>Liver Neoplasms - mortality</topic><topic>Liver Neoplasms - pathology</topic><topic>Male</topic><topic>Medical prognosis</topic><topic>Mesenchyme</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Mice</topic><topic>Middle Aged</topic><topic>Multivariate Analysis</topic><topic>Neoplasm Invasiveness - pathology</topic><topic>Neoplasm Metastasis - genetics</topic><topic>Notch1 protein</topic><topic>Phenylglycine</topic><topic>Predictive Value of Tests</topic><topic>Prognosis</topic><topic>Random Allocation</topic><topic>Survival Analysis</topic><topic>Transcriptional Activation</topic><topic>Tumor Cells, Cultured</topic><topic>Up-Regulation</topic><topic>Xenografts</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xiao, Shuai</creatorcontrib><creatorcontrib>Chang, Rui‐Min</creatorcontrib><creatorcontrib>Yang, Ming‐Yang</creatorcontrib><creatorcontrib>Lei, Xiong</creatorcontrib><creatorcontrib>Liu, Xiao</creatorcontrib><creatorcontrib>Gao, Wen‐Bin</creatorcontrib><creatorcontrib>Xiao, Jing‐Lei</creatorcontrib><creatorcontrib>Yang, Lian‐Yue</creatorcontrib><collection>Wiley Online Library (Open Access Collection)</collection><collection>Wiley Online Library Free Content</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Hepatology (Baltimore, Md.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xiao, Shuai</au><au>Chang, Rui‐Min</au><au>Yang, Ming‐Yang</au><au>Lei, Xiong</au><au>Liu, Xiao</au><au>Gao, Wen‐Bin</au><au>Xiao, Jing‐Lei</au><au>Yang, Lian‐Yue</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Actin‐like 6A predicts poor prognosis of hepatocellular carcinoma and promotes metastasis and epithelial‐mesenchymal transition</atitle><jtitle>Hepatology (Baltimore, Md.)</jtitle><addtitle>Hepatology</addtitle><date>2016-04</date><risdate>2016</risdate><volume>63</volume><issue>4</issue><spage>1256</spage><epage>1271</epage><pages>1256-1271</pages><issn>0270-9139</issn><eissn>1527-3350</eissn><coden>HPTLD9</coden><abstract>Hepatocellular carcinoma (HCC) is one of the most lethal cancers worldwide because of metastasis. Epithelial‐mesenchymal transition (EMT) is widely considered to be crucial to the invasion‐metastasis cascade during cancer progression. Actin‐like 6A (ACTL6A) is initially verified important for cell proliferation, differentiation, and migration. In this study, we find that ACTL6A plays an essential role in metastasis and EMT of HCC. ACTL6A expression is up‐regulated in HCC cells and tissues. A high level of ACTL6A in HCCs is correlated with aggressive clinicopathological features and is an independent poor prognostic factor for overall and disease‐free survival of HCC patients. Ectopic expression of ACTL6A markedly promotes HCC cells migration, invasion, as well as EMT in vitro and promotes tumor growth and metastasis in the mouse xenograft model. Opposite results are observed when ACTL6A is knocked down. Mechanistically, ACTL6A promotes metastasis and EMT through activating Notch signaling. ACTL6A knockdown has the equal blockage effect as the Notch signaling inhibitor, N‐[N‐(3,5‐difluorophenacetyl)‐L‐alanyl]‐S‐phenylglycine t‐butylester, in HCC cells. Further studies indicate that ACTL6A might manipulate SRY (sex determining region Y)‐box 2 (SOX2) expression and then activate Notch1 signaling. Conclusions: ACTL6A promotes metastasis and EMT by SOX2/Notch1 signaling, indicating a prognostic biomarker candidate and a potential therapeutic target for HCC. (Hepatology 2016;63:1256–1271)</abstract><cop>United States</cop><pub>Wolters Kluwer Health, Inc</pub><pmid>26698646</pmid><doi>10.1002/hep.28417</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Actin Actins - genetics Adult Aged Analysis of Variance Animals Biopsy, Needle Carcinoma, Hepatocellular - genetics Carcinoma, Hepatocellular - mortality Carcinoma, Hepatocellular - pathology Cell adhesion & migration Cell migration Cell proliferation Chromosomal Proteins, Non-Histone - genetics Disease Models, Animal DNA-Binding Proteins - genetics Ectopic expression Epithelial-Mesenchymal Transition - genetics Female Gene Expression Regulation, Neoplastic Hepatobiliary Malignancies Hepatocellular carcinoma Hepatology Humans Immunohistochemistry Liver cancer Liver Neoplasms - genetics Liver Neoplasms - mortality Liver Neoplasms - pathology Male Medical prognosis Mesenchyme Metastases Metastasis Mice Middle Aged Multivariate Analysis Neoplasm Invasiveness - pathology Neoplasm Metastasis - genetics Notch1 protein Phenylglycine Predictive Value of Tests Prognosis Random Allocation Survival Analysis Transcriptional Activation Tumor Cells, Cultured Up-Regulation Xenografts |
| title | Actin‐like 6A predicts poor prognosis of hepatocellular carcinoma and promotes metastasis and epithelial‐mesenchymal transition |
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