Inhibitor of [beta]-catenin and TCF (ICAT) promotes cervical cancer growth and metastasis by disrupting E-cadherin/[beta]-catenin complex
The inhibitor of [beta]-catenin and TCF (ICAT) blocks the binding of TCF to [beta]-catenin and has been demonstrated as a suppressor of the Wnt/[beta]-catenin signaling pathway. It has been reported to exert a different function around a wide variety of cancers. However, its function and underlying...
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| Veröffentlicht in: | Oncology reports 2017-11, Vol.38 (5), p.2597 |
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| container_title | Oncology reports |
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| creator | Jiang, Yayun Ren, Wei Wang, Weijia Xia, Jing Gou, Liyao Liu, Mengyao Wan, Qun Zhou, Lan Weng, Yaguang He, Tongchuan Zhang, Yan |
| description | The inhibitor of [beta]-catenin and TCF (ICAT) blocks the binding of TCF to [beta]-catenin and has been demonstrated as a suppressor of the Wnt/[beta]-catenin signaling pathway. It has been reported to exert a different function around a wide variety of cancers. However, its function and underlying mechanisms in human cervical cancer remains unknown. In the present study, the expression of ICAT in 41 human cervical cancer tissues and 30 normal cervical tissues was evaluated by immunohistochemical analysis. ICAT was found highly expressed in cancer tissues. ICAT overexpression significantly promoted SiHa cell proliferation in vitro by causing Gl arrest, and enhanced cell migration and invasion whereas, ICAT knockdown induced opposite effects in Caski cells which have higher expression of ICAT. Downregulation or overexpression of ICAT resulted in an altered expression of the epithelial-mesenchymal transition (EMT). Furthermore, immunoprecipitation assays revealed that ICAT pormoted cervical cancer EMT by competing in E-cadhenin binding to [beta]-caterin. Overexpression of ICAT in SiHa cells promoted tumor growth and EMT was also demonstrated by the xenograft mouse experiment. These results demonstrate that ICAT contributed to the progression of cervical cancer and may play a role in the regulation of EMT by distrupting the E-cadherin/[beta]-catenin complex. It may be a novel potential therapeutic target for therapy in human cervical cancer. |
| doi_str_mv | 10.3892/or.2017.5962 |
| format | Article |
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It has been reported to exert a different function around a wide variety of cancers. However, its function and underlying mechanisms in human cervical cancer remains unknown. In the present study, the expression of ICAT in 41 human cervical cancer tissues and 30 normal cervical tissues was evaluated by immunohistochemical analysis. ICAT was found highly expressed in cancer tissues. ICAT overexpression significantly promoted SiHa cell proliferation in vitro by causing Gl arrest, and enhanced cell migration and invasion whereas, ICAT knockdown induced opposite effects in Caski cells which have higher expression of ICAT. Downregulation or overexpression of ICAT resulted in an altered expression of the epithelial-mesenchymal transition (EMT). Furthermore, immunoprecipitation assays revealed that ICAT pormoted cervical cancer EMT by competing in E-cadhenin binding to [beta]-caterin. Overexpression of ICAT in SiHa cells promoted tumor growth and EMT was also demonstrated by the xenograft mouse experiment. These results demonstrate that ICAT contributed to the progression of cervical cancer and may play a role in the regulation of EMT by distrupting the E-cadherin/[beta]-catenin complex. It may be a novel potential therapeutic target for therapy in human cervical cancer.</description><identifier>ISSN: 1021-335X</identifier><identifier>DOI: 10.3892/or.2017.5962</identifier><language>eng</language><publisher>Spandidos Publications</publisher><subject>Cancer metastasis ; Cervical cancer ; Development and progression ; Gene expression ; Genetic aspects</subject><ispartof>Oncology reports, 2017-11, Vol.38 (5), p.2597</ispartof><rights>COPYRIGHT 2017 Spandidos Publications</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,782,786,27931,27932</link.rule.ids></links><search><creatorcontrib>Jiang, Yayun</creatorcontrib><creatorcontrib>Ren, Wei</creatorcontrib><creatorcontrib>Wang, Weijia</creatorcontrib><creatorcontrib>Xia, Jing</creatorcontrib><creatorcontrib>Gou, Liyao</creatorcontrib><creatorcontrib>Liu, Mengyao</creatorcontrib><creatorcontrib>Wan, Qun</creatorcontrib><creatorcontrib>Zhou, Lan</creatorcontrib><creatorcontrib>Weng, Yaguang</creatorcontrib><creatorcontrib>He, Tongchuan</creatorcontrib><creatorcontrib>Zhang, Yan</creatorcontrib><title>Inhibitor of [beta]-catenin and TCF (ICAT) promotes cervical cancer growth and metastasis by disrupting E-cadherin/[beta]-catenin complex</title><title>Oncology reports</title><description>The inhibitor of [beta]-catenin and TCF (ICAT) blocks the binding of TCF to [beta]-catenin and has been demonstrated as a suppressor of the Wnt/[beta]-catenin signaling pathway. It has been reported to exert a different function around a wide variety of cancers. However, its function and underlying mechanisms in human cervical cancer remains unknown. In the present study, the expression of ICAT in 41 human cervical cancer tissues and 30 normal cervical tissues was evaluated by immunohistochemical analysis. ICAT was found highly expressed in cancer tissues. ICAT overexpression significantly promoted SiHa cell proliferation in vitro by causing Gl arrest, and enhanced cell migration and invasion whereas, ICAT knockdown induced opposite effects in Caski cells which have higher expression of ICAT. Downregulation or overexpression of ICAT resulted in an altered expression of the epithelial-mesenchymal transition (EMT). Furthermore, immunoprecipitation assays revealed that ICAT pormoted cervical cancer EMT by competing in E-cadhenin binding to [beta]-caterin. Overexpression of ICAT in SiHa cells promoted tumor growth and EMT was also demonstrated by the xenograft mouse experiment. These results demonstrate that ICAT contributed to the progression of cervical cancer and may play a role in the regulation of EMT by distrupting the E-cadherin/[beta]-catenin complex. It may be a novel potential therapeutic target for therapy in human cervical cancer.</description><subject>Cancer metastasis</subject><subject>Cervical cancer</subject><subject>Development and progression</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><issn>1021-335X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid/><recordid>eNptjUtLAzEUhbNQsFZ3_oCAILqYaR7zXJbSaqHgZhaCSMnkMROZSUqS-vgJ_muDuqgi98I9XL5zDgAXGKW0qsnMupQgXKZ5XZAjMMGI4ITS_OEEnHr_jBApUVFPwMfa9LrVwTpoFXxsZWBPCWdBGm0gMwI2ixW8Xi_mzQ3cOTvaID3k0r1ozgbImYkads6-hv4LH2OAj6s9bN-h0N7td0GbDi5jquil02b2p4XbcTfItzNwrNjg5fnPnYJmtWwWd8nm_jb2b5KurlCCUSYKLlQlactKInIhKBMlQ1hyxCkmLVIZK3CuCC0KSlleK5xVrGwlYYJiOgWX37EdG-RWG2WDY3zUnm_nOckySjKKIpX-Q8URctTcGql0_P8yXB0YesmG0Hs77IO2xh-Cn51Yfz8</recordid><startdate>20171101</startdate><enddate>20171101</enddate><creator>Jiang, Yayun</creator><creator>Ren, Wei</creator><creator>Wang, Weijia</creator><creator>Xia, Jing</creator><creator>Gou, Liyao</creator><creator>Liu, Mengyao</creator><creator>Wan, Qun</creator><creator>Zhou, Lan</creator><creator>Weng, Yaguang</creator><creator>He, Tongchuan</creator><creator>Zhang, Yan</creator><general>Spandidos Publications</general><scope/></search><sort><creationdate>20171101</creationdate><title>Inhibitor of [beta]-catenin and TCF (ICAT) promotes cervical cancer growth and metastasis by disrupting E-cadherin/[beta]-catenin complex</title><author>Jiang, Yayun ; Ren, Wei ; Wang, Weijia ; Xia, Jing ; Gou, Liyao ; Liu, Mengyao ; Wan, Qun ; Zhou, Lan ; Weng, Yaguang ; He, Tongchuan ; Zhang, Yan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-g980-104d6cdf8e3ba72d5dd3ad7a01ec0c312b0f4a615f236633a59f148a7be2ad313</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Cancer metastasis</topic><topic>Cervical cancer</topic><topic>Development and progression</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><toplevel>online_resources</toplevel><creatorcontrib>Jiang, Yayun</creatorcontrib><creatorcontrib>Ren, Wei</creatorcontrib><creatorcontrib>Wang, Weijia</creatorcontrib><creatorcontrib>Xia, Jing</creatorcontrib><creatorcontrib>Gou, Liyao</creatorcontrib><creatorcontrib>Liu, Mengyao</creatorcontrib><creatorcontrib>Wan, Qun</creatorcontrib><creatorcontrib>Zhou, Lan</creatorcontrib><creatorcontrib>Weng, Yaguang</creatorcontrib><creatorcontrib>He, Tongchuan</creatorcontrib><creatorcontrib>Zhang, Yan</creatorcontrib><jtitle>Oncology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jiang, Yayun</au><au>Ren, Wei</au><au>Wang, Weijia</au><au>Xia, Jing</au><au>Gou, Liyao</au><au>Liu, Mengyao</au><au>Wan, Qun</au><au>Zhou, Lan</au><au>Weng, Yaguang</au><au>He, Tongchuan</au><au>Zhang, Yan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibitor of [beta]-catenin and TCF (ICAT) promotes cervical cancer growth and metastasis by disrupting E-cadherin/[beta]-catenin complex</atitle><jtitle>Oncology reports</jtitle><date>2017-11-01</date><risdate>2017</risdate><volume>38</volume><issue>5</issue><spage>2597</spage><pages>2597-</pages><issn>1021-335X</issn><abstract>The inhibitor of [beta]-catenin and TCF (ICAT) blocks the binding of TCF to [beta]-catenin and has been demonstrated as a suppressor of the Wnt/[beta]-catenin signaling pathway. It has been reported to exert a different function around a wide variety of cancers. However, its function and underlying mechanisms in human cervical cancer remains unknown. In the present study, the expression of ICAT in 41 human cervical cancer tissues and 30 normal cervical tissues was evaluated by immunohistochemical analysis. ICAT was found highly expressed in cancer tissues. ICAT overexpression significantly promoted SiHa cell proliferation in vitro by causing Gl arrest, and enhanced cell migration and invasion whereas, ICAT knockdown induced opposite effects in Caski cells which have higher expression of ICAT. Downregulation or overexpression of ICAT resulted in an altered expression of the epithelial-mesenchymal transition (EMT). Furthermore, immunoprecipitation assays revealed that ICAT pormoted cervical cancer EMT by competing in E-cadhenin binding to [beta]-caterin. Overexpression of ICAT in SiHa cells promoted tumor growth and EMT was also demonstrated by the xenograft mouse experiment. These results demonstrate that ICAT contributed to the progression of cervical cancer and may play a role in the regulation of EMT by distrupting the E-cadherin/[beta]-catenin complex. It may be a novel potential therapeutic target for therapy in human cervical cancer.</abstract><pub>Spandidos Publications</pub><doi>10.3892/or.2017.5962</doi></addata></record> |
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| ispartof | Oncology reports, 2017-11, Vol.38 (5), p.2597 |
| issn | 1021-335X |
| language | eng |
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| source | EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Cancer metastasis Cervical cancer Development and progression Gene expression Genetic aspects |
| title | Inhibitor of [beta]-catenin and TCF (ICAT) promotes cervical cancer growth and metastasis by disrupting E-cadherin/[beta]-catenin complex |
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