P-Akt/miR-200 signaling regulates epithelial-mesenchymal transition, migration and invasion in circulating gastric tumor cells
Both circulating tumor cells (CTCs) and epithelial-mesenchymal transition (EMT) play an important role in invasion, migration and chemoresistant in tumor development. This study aimed to detect whether EMT occurred in human gastric CTCs and to explore the mechanism of EMT in human gastric CTCs. We a...
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| Veröffentlicht in: | International journal of oncology 2014-12, Vol.45 (6), p.2430-2438 |
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| creator | YUAN, DANDAN XIA, HONGWEI ZHANG, YUCHEN CHEN, LIANG LENG, WEIBING CHEN, TIE CHEN, QINGJUAN TANG, QIULIN MO, XIANMING LIU, MING BI, FENG |
| description | Both circulating tumor cells (CTCs) and epithelial-mesenchymal transition (EMT) play an important role in invasion, migration and chemoresistant in tumor development. This study aimed to detect whether EMT occurred in human gastric CTCs and to explore the mechanism of EMT in human gastric CTCs. We analysed epithelial markers (pan-CK, E-cadherin), mesenchymal markers (N-cadherin, vimentin) EMT related miR-200s, and Akt in gastric CTCs. The impact of miR-200s on EMT, migration and invasion in CTCs was tested. We found that epithelial markers pan-CK, E-cadherin were decreased, and mesenchymal markers N-cadherin, vimentin were overexpressed in gastric CTCs. Expression of EMT related transcriptors, snail1, zeb1, twist1, were reversely correlated with miR-200s, and were positively correlated with phospho-Akt. Upregulated of miR-200s downregulated twist1 and zeb1 mRNA expression, and resulted in the supression of EMT, and impaired migration and invasion in gastric CTCs. Inhibition of p-Akt led to upregulation of miR-200s. In conclusion, gastric CTCs exhibited remarkable EMT process, and p-Akt/miR-200s signaling regulates EMT, migration and invasion in gastric CTCs. |
| doi_str_mv | 10.3892/ijo.2014.2644 |
| format | Article |
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This study aimed to detect whether EMT occurred in human gastric CTCs and to explore the mechanism of EMT in human gastric CTCs. We analysed epithelial markers (pan-CK, E-cadherin), mesenchymal markers (N-cadherin, vimentin) EMT related miR-200s, and Akt in gastric CTCs. The impact of miR-200s on EMT, migration and invasion in CTCs was tested. We found that epithelial markers pan-CK, E-cadherin were decreased, and mesenchymal markers N-cadherin, vimentin were overexpressed in gastric CTCs. Expression of EMT related transcriptors, snail1, zeb1, twist1, were reversely correlated with miR-200s, and were positively correlated with phospho-Akt. Upregulated of miR-200s downregulated twist1 and zeb1 mRNA expression, and resulted in the supression of EMT, and impaired migration and invasion in gastric CTCs. Inhibition of p-Akt led to upregulation of miR-200s. In conclusion, gastric CTCs exhibited remarkable EMT process, and p-Akt/miR-200s signaling regulates EMT, migration and invasion in gastric CTCs.</description><identifier>ISSN: 1019-6439</identifier><identifier>EISSN: 1791-2423</identifier><identifier>DOI: 10.3892/ijo.2014.2644</identifier><identifier>PMID: 25200917</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Biomarkers, Tumor - biosynthesis ; Breast cancer ; Cancer cells ; Cancer therapies ; Cell adhesion & migration ; Cell Line, Tumor ; Cell Movement - genetics ; circulating tumor cells ; Development and progression ; epithelial-mesenchymal transition ; Epithelial-Mesenchymal Transition - genetics ; Esophagus ; Gastric cancer ; Gene Expression Regulation, Neoplastic ; Genetic aspects ; Humans ; Infrared imaging systems ; Metastasis ; MicroRNA ; MicroRNAs - biosynthesis ; MicroRNAs - genetics ; miR-200s ; Neoplasm Invasiveness - genetics ; Neoplasm Proteins - biosynthesis ; Neoplastic Cells, Circulating - metabolism ; Neoplastic Cells, Circulating - pathology ; Oncogene Protein v-akt - biosynthesis ; Oncogene Protein v-akt - genetics ; p-Akt ; Physiological aspects ; Prostate cancer ; Stomach cancer ; Stomach Neoplasms - genetics ; Stomach Neoplasms - pathology</subject><ispartof>International journal of oncology, 2014-12, Vol.45 (6), p.2430-2438</ispartof><rights>Copyright © 2014, Spandidos Publications</rights><rights>COPYRIGHT 2014 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c490t-14ce0744bb174f1125b4d3a31b8897f06efe04dd77cc7802194df616e24b2c213</citedby><cites>FETCH-LOGICAL-c490t-14ce0744bb174f1125b4d3a31b8897f06efe04dd77cc7802194df616e24b2c213</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,5570,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25200917$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>YUAN, DANDAN</creatorcontrib><creatorcontrib>XIA, HONGWEI</creatorcontrib><creatorcontrib>ZHANG, YUCHEN</creatorcontrib><creatorcontrib>CHEN, LIANG</creatorcontrib><creatorcontrib>LENG, WEIBING</creatorcontrib><creatorcontrib>CHEN, TIE</creatorcontrib><creatorcontrib>CHEN, QINGJUAN</creatorcontrib><creatorcontrib>TANG, QIULIN</creatorcontrib><creatorcontrib>MO, XIANMING</creatorcontrib><creatorcontrib>LIU, MING</creatorcontrib><creatorcontrib>BI, FENG</creatorcontrib><title>P-Akt/miR-200 signaling regulates epithelial-mesenchymal transition, migration and invasion in circulating gastric tumor cells</title><title>International journal of oncology</title><addtitle>Int J Oncol</addtitle><description>Both circulating tumor cells (CTCs) and epithelial-mesenchymal transition (EMT) play an important role in invasion, migration and chemoresistant in tumor development. This study aimed to detect whether EMT occurred in human gastric CTCs and to explore the mechanism of EMT in human gastric CTCs. We analysed epithelial markers (pan-CK, E-cadherin), mesenchymal markers (N-cadherin, vimentin) EMT related miR-200s, and Akt in gastric CTCs. The impact of miR-200s on EMT, migration and invasion in CTCs was tested. We found that epithelial markers pan-CK, E-cadherin were decreased, and mesenchymal markers N-cadherin, vimentin were overexpressed in gastric CTCs. Expression of EMT related transcriptors, snail1, zeb1, twist1, were reversely correlated with miR-200s, and were positively correlated with phospho-Akt. Upregulated of miR-200s downregulated twist1 and zeb1 mRNA expression, and resulted in the supression of EMT, and impaired migration and invasion in gastric CTCs. Inhibition of p-Akt led to upregulation of miR-200s. In conclusion, gastric CTCs exhibited remarkable EMT process, and p-Akt/miR-200s signaling regulates EMT, migration and invasion in gastric CTCs.</description><subject>Biomarkers, Tumor - biosynthesis</subject><subject>Breast cancer</subject><subject>Cancer cells</subject><subject>Cancer therapies</subject><subject>Cell adhesion & migration</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - genetics</subject><subject>circulating tumor cells</subject><subject>Development and progression</subject><subject>epithelial-mesenchymal transition</subject><subject>Epithelial-Mesenchymal Transition - genetics</subject><subject>Esophagus</subject><subject>Gastric cancer</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genetic aspects</subject><subject>Humans</subject><subject>Infrared imaging systems</subject><subject>Metastasis</subject><subject>MicroRNA</subject><subject>MicroRNAs - biosynthesis</subject><subject>MicroRNAs - genetics</subject><subject>miR-200s</subject><subject>Neoplasm Invasiveness - genetics</subject><subject>Neoplasm Proteins - biosynthesis</subject><subject>Neoplastic Cells, Circulating - metabolism</subject><subject>Neoplastic Cells, Circulating - pathology</subject><subject>Oncogene Protein v-akt - biosynthesis</subject><subject>Oncogene Protein v-akt - genetics</subject><subject>p-Akt</subject><subject>Physiological aspects</subject><subject>Prostate cancer</subject><subject>Stomach cancer</subject><subject>Stomach Neoplasms - genetics</subject><subject>Stomach Neoplasms - pathology</subject><issn>1019-6439</issn><issn>1791-2423</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkstrFTEUxgex2FpdupWAoBtzm9e8lpfio1BQRNchk8nMPdc8rklG6Ma_vRluLS2ULHLO4Xc--PKlqt5QsuFdzy5gHzaMULFhjRDPqjPa9hQzwfjzUhPa40bw_rR6mdKeEFbXhL6oTlnNCOlpe1b9-463v_OFgx-4jFCC2SsLfkbRzItV2SRkDpB3xoKy2JlkvN7dOGVRjsonyBD8R-RgjmotkfIjAv9XpbUBjzREveqskrNKOYJGeXEhIm2sTa-qk0nZZF7f3efVr8-ffl5-xdffvlxdbq-xFj3JmAptSCvEMNBWTJSyehAjV5wOXde3E2nMZIgYx7bVuu0Io70Yp4Y2homBaUb5efXuqHuI4c9iUpb7sMRiNUnac8Y5qbsH1KyskeCnUExqB0nLrSCUd4Vihdo8QZUzGgc6eDNBmT9aeP9gYWeUzbsU7LI-WHoM4iOoY0gpmkkeIjgVbyQlck1blrTlmrZc0y782ztXy-DMeE__j7cAH45AOpRgYAzpnilKWNSYNOWzcMJvARJMsOA</recordid><startdate>20141201</startdate><enddate>20141201</enddate><creator>YUAN, DANDAN</creator><creator>XIA, HONGWEI</creator><creator>ZHANG, YUCHEN</creator><creator>CHEN, LIANG</creator><creator>LENG, WEIBING</creator><creator>CHEN, TIE</creator><creator>CHEN, QINGJUAN</creator><creator>TANG, QIULIN</creator><creator>MO, XIANMING</creator><creator>LIU, MING</creator><creator>BI, FENG</creator><general>D.A. 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This study aimed to detect whether EMT occurred in human gastric CTCs and to explore the mechanism of EMT in human gastric CTCs. We analysed epithelial markers (pan-CK, E-cadherin), mesenchymal markers (N-cadherin, vimentin) EMT related miR-200s, and Akt in gastric CTCs. The impact of miR-200s on EMT, migration and invasion in CTCs was tested. We found that epithelial markers pan-CK, E-cadherin were decreased, and mesenchymal markers N-cadherin, vimentin were overexpressed in gastric CTCs. Expression of EMT related transcriptors, snail1, zeb1, twist1, were reversely correlated with miR-200s, and were positively correlated with phospho-Akt. Upregulated of miR-200s downregulated twist1 and zeb1 mRNA expression, and resulted in the supression of EMT, and impaired migration and invasion in gastric CTCs. Inhibition of p-Akt led to upregulation of miR-200s. In conclusion, gastric CTCs exhibited remarkable EMT process, and p-Akt/miR-200s signaling regulates EMT, migration and invasion in gastric CTCs.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>25200917</pmid><doi>10.3892/ijo.2014.2644</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Biomarkers, Tumor - biosynthesis Breast cancer Cancer cells Cancer therapies Cell adhesion & migration Cell Line, Tumor Cell Movement - genetics circulating tumor cells Development and progression epithelial-mesenchymal transition Epithelial-Mesenchymal Transition - genetics Esophagus Gastric cancer Gene Expression Regulation, Neoplastic Genetic aspects Humans Infrared imaging systems Metastasis MicroRNA MicroRNAs - biosynthesis MicroRNAs - genetics miR-200s Neoplasm Invasiveness - genetics Neoplasm Proteins - biosynthesis Neoplastic Cells, Circulating - metabolism Neoplastic Cells, Circulating - pathology Oncogene Protein v-akt - biosynthesis Oncogene Protein v-akt - genetics p-Akt Physiological aspects Prostate cancer Stomach cancer Stomach Neoplasms - genetics Stomach Neoplasms - pathology |
| title | P-Akt/miR-200 signaling regulates epithelial-mesenchymal transition, migration and invasion in circulating gastric tumor cells |
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