α-Actinin-4 induces the epithelial-to-mesenchymal transition and tumorigenesis via regulation of Snail expression and β-catenin stabilization in cervical cancer
α-Actinin-4 (ACTN4) is frequently amplified and overexpressed in various cancers. Although ACTN4 functions in cancer cell migration and invasion, the roles of ACTN4 during the epithelial-to-mesenchymal transition (EMT) and cervical cancer tumorigenesis are unknown. In this study, we investigated the...
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| Veröffentlicht in: | Oncogene 2016-11, Vol.35 (45), p.5893-5904 |
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| description | α-Actinin-4 (ACTN4) is frequently amplified and overexpressed in various cancers. Although ACTN4 functions in cancer cell migration and invasion, the roles of ACTN4 during the epithelial-to-mesenchymal transition (EMT) and cervical cancer tumorigenesis are unknown. In this study, we investigated the function of ACTN4 in the progression of cervical cancer and the mechanisms of EMT and tumorigenesis induced by ACTN4. We found that ACTN4 induced EMT by upregulating Snail, which was dependent on the Akt signaling pathway in cervical cancer. ACTN4 induced cell migration and invasion through Snail-mediated matrix metalloproteinase-9 expression. ACTN4 expression level was correlated with stabilization of β-catenin. Accumulatioin of β-catenin owing to ACTN4 induced tumorigenesis via upregulation of genes involved in cell proliferation, including cyclin D1 and c-myc. ACTN4 knockdown reduced cervical cancer cell proliferation and tumor formation
in vivo
. The expression level of ACTN4 is highly elevated in human cervical tumors, compared with that in normal cervical tissues. ACTN4-overexpressing MDCK cells induced tumor formation and metastatic nodules in nude mice. Our findings indicate that ACTN4 promotes EMT and tumorigenesis by regulating Snail expression and the Akt pathway in cervical cancer. We propose a novel mechanism for EMT and tumorigenesis in cervical cancer. |
| doi_str_mv | 10.1038/onc.2016.117 |
| format | Article |
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in vivo
. The expression level of ACTN4 is highly elevated in human cervical tumors, compared with that in normal cervical tissues. ACTN4-overexpressing MDCK cells induced tumor formation and metastatic nodules in nude mice. Our findings indicate that ACTN4 promotes EMT and tumorigenesis by regulating Snail expression and the Akt pathway in cervical cancer. We propose a novel mechanism for EMT and tumorigenesis in cervical cancer.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/onc.2016.117</identifier><identifier>PMID: 27065319</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/1 ; 13/51 ; 13/95 ; 14/105 ; 14/19 ; 42/89 ; 631/67/1517/1371 ; 631/67/1857 ; 82/29 ; 96/106 ; Actinin ; Actinin - genetics ; Actinin - metabolism ; AKT protein ; Animals ; Apoptosis ; beta Catenin - metabolism ; c-Myc protein ; Cell adhesion & migration ; Cell Biology ; Cell growth ; Cell Line ; Cell Line, Tumor ; Cell migration ; Cell Movement ; Cell Proliferation ; Cell Transformation, Neoplastic - genetics ; Cell Transformation, Neoplastic - metabolism ; Cervical cancer ; Cervix ; Cyclin D1 ; Disease Models, Animal ; Epithelial-Mesenchymal Transition - genetics ; Female ; Gene Expression ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Genes, Reporter ; Human Genetics ; Humans ; Internal Medicine ; Male ; Matrix metalloproteinase ; Matrix Metalloproteinase 9 - metabolism ; Medicine ; Medicine & Public Health ; Mesenchyme ; Metalloproteinase ; Metastases ; Mice ; Myc protein ; Oncology ; original-article ; Protein Stability ; Proto-Oncogene Proteins c-akt - metabolism ; Signal transduction ; Snail Family Transcription Factors - genetics ; Tumorigenesis ; Uterine Cervical Neoplasms - genetics ; Uterine Cervical Neoplasms - metabolism ; Uterine Cervical Neoplasms - pathology ; Xenograft Model Antitumor Assays ; β-Catenin</subject><ispartof>Oncogene, 2016-11, Vol.35 (45), p.5893-5904</ispartof><rights>Macmillan Publishers Limited 2016</rights><rights>Macmillan Publishers Limited 2016.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c428t-d3cd90eef2b682c04731dd1dde577163c8b07a4900fffc8db0d2a1150ecf84a03</citedby><cites>FETCH-LOGICAL-c428t-d3cd90eef2b682c04731dd1dde577163c8b07a4900fffc8db0d2a1150ecf84a03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/onc.2016.117$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/onc.2016.117$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27065319$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>An, H-T</creatorcontrib><creatorcontrib>Yoo, S</creatorcontrib><creatorcontrib>Ko, J</creatorcontrib><title>α-Actinin-4 induces the epithelial-to-mesenchymal transition and tumorigenesis via regulation of Snail expression and β-catenin stabilization in cervical cancer</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>α-Actinin-4 (ACTN4) is frequently amplified and overexpressed in various cancers. Although ACTN4 functions in cancer cell migration and invasion, the roles of ACTN4 during the epithelial-to-mesenchymal transition (EMT) and cervical cancer tumorigenesis are unknown. In this study, we investigated the function of ACTN4 in the progression of cervical cancer and the mechanisms of EMT and tumorigenesis induced by ACTN4. We found that ACTN4 induced EMT by upregulating Snail, which was dependent on the Akt signaling pathway in cervical cancer. ACTN4 induced cell migration and invasion through Snail-mediated matrix metalloproteinase-9 expression. ACTN4 expression level was correlated with stabilization of β-catenin. Accumulatioin of β-catenin owing to ACTN4 induced tumorigenesis via upregulation of genes involved in cell proliferation, including cyclin D1 and c-myc. ACTN4 knockdown reduced cervical cancer cell proliferation and tumor formation
in vivo
. The expression level of ACTN4 is highly elevated in human cervical tumors, compared with that in normal cervical tissues. ACTN4-overexpressing MDCK cells induced tumor formation and metastatic nodules in nude mice. Our findings indicate that ACTN4 promotes EMT and tumorigenesis by regulating Snail expression and the Akt pathway in cervical cancer. We propose a novel mechanism for EMT and tumorigenesis in cervical cancer.</description><subject>13/1</subject><subject>13/51</subject><subject>13/95</subject><subject>14/105</subject><subject>14/19</subject><subject>42/89</subject><subject>631/67/1517/1371</subject><subject>631/67/1857</subject><subject>82/29</subject><subject>96/106</subject><subject>Actinin</subject><subject>Actinin - genetics</subject><subject>Actinin - metabolism</subject><subject>AKT protein</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>beta Catenin - metabolism</subject><subject>c-Myc protein</subject><subject>Cell adhesion & migration</subject><subject>Cell Biology</subject><subject>Cell growth</subject><subject>Cell Line</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Cell Transformation, Neoplastic - genetics</subject><subject>Cell Transformation, Neoplastic - metabolism</subject><subject>Cervical cancer</subject><subject>Cervix</subject><subject>Cyclin D1</subject><subject>Disease Models, Animal</subject><subject>Epithelial-Mesenchymal Transition - 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Academic</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>An, H-T</au><au>Yoo, S</au><au>Ko, J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>α-Actinin-4 induces the epithelial-to-mesenchymal transition and tumorigenesis via regulation of Snail expression and β-catenin stabilization in cervical cancer</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2016-11-10</date><risdate>2016</risdate><volume>35</volume><issue>45</issue><spage>5893</spage><epage>5904</epage><pages>5893-5904</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><abstract>α-Actinin-4 (ACTN4) is frequently amplified and overexpressed in various cancers. Although ACTN4 functions in cancer cell migration and invasion, the roles of ACTN4 during the epithelial-to-mesenchymal transition (EMT) and cervical cancer tumorigenesis are unknown. In this study, we investigated the function of ACTN4 in the progression of cervical cancer and the mechanisms of EMT and tumorigenesis induced by ACTN4. We found that ACTN4 induced EMT by upregulating Snail, which was dependent on the Akt signaling pathway in cervical cancer. ACTN4 induced cell migration and invasion through Snail-mediated matrix metalloproteinase-9 expression. ACTN4 expression level was correlated with stabilization of β-catenin. Accumulatioin of β-catenin owing to ACTN4 induced tumorigenesis via upregulation of genes involved in cell proliferation, including cyclin D1 and c-myc. ACTN4 knockdown reduced cervical cancer cell proliferation and tumor formation
in vivo
. The expression level of ACTN4 is highly elevated in human cervical tumors, compared with that in normal cervical tissues. ACTN4-overexpressing MDCK cells induced tumor formation and metastatic nodules in nude mice. Our findings indicate that ACTN4 promotes EMT and tumorigenesis by regulating Snail expression and the Akt pathway in cervical cancer. We propose a novel mechanism for EMT and tumorigenesis in cervical cancer.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>27065319</pmid><doi>10.1038/onc.2016.117</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 13/1 13/51 13/95 14/105 14/19 42/89 631/67/1517/1371 631/67/1857 82/29 96/106 Actinin Actinin - genetics Actinin - metabolism AKT protein Animals Apoptosis beta Catenin - metabolism c-Myc protein Cell adhesion & migration Cell Biology Cell growth Cell Line Cell Line, Tumor Cell migration Cell Movement Cell Proliferation Cell Transformation, Neoplastic - genetics Cell Transformation, Neoplastic - metabolism Cervical cancer Cervix Cyclin D1 Disease Models, Animal Epithelial-Mesenchymal Transition - genetics Female Gene Expression Gene Expression Regulation, Neoplastic Gene Knockdown Techniques Genes, Reporter Human Genetics Humans Internal Medicine Male Matrix metalloproteinase Matrix Metalloproteinase 9 - metabolism Medicine Medicine & Public Health Mesenchyme Metalloproteinase Metastases Mice Myc protein Oncology original-article Protein Stability Proto-Oncogene Proteins c-akt - metabolism Signal transduction Snail Family Transcription Factors - genetics Tumorigenesis Uterine Cervical Neoplasms - genetics Uterine Cervical Neoplasms - metabolism Uterine Cervical Neoplasms - pathology Xenograft Model Antitumor Assays β-Catenin |
| title | α-Actinin-4 induces the epithelial-to-mesenchymal transition and tumorigenesis via regulation of Snail expression and β-catenin stabilization in cervical cancer |
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