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MicroRNA-194 Inhibits the Epithelial–Mesenchymal Transition in Gastric Cancer Cells by Targeting FoxM1
Aim We hypothesized that miR-194 may control Forkhead box protein M1 (FoxM1) expression in gastric cancer cells and therefore may have therapeutic potential in gastric cancer. Methods The expression level of miR-194 was examined using real-time PCR in human gastric cancer and noncancerous gastric ti...
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Published in: | Digestive diseases and sciences 2014-09, Vol.59 (9), p.2145-2152 |
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container_end_page | 2152 |
container_issue | 9 |
container_start_page | 2145 |
container_title | Digestive diseases and sciences |
container_volume | 59 |
creator | Li, Zhenjun Ying, Xiaojiang Chen, Hongliang Ye, Pingjiang Shen, Yi Pan, Weihuo Zhang, Lihua |
description | Aim
We hypothesized that miR-194 may control Forkhead box protein M1 (FoxM1) expression in gastric cancer cells and therefore may have therapeutic potential in gastric cancer.
Methods
The expression level of miR-194 was examined using real-time PCR in human gastric cancer and noncancerous gastric tissues, gastric cancer cell and normal gastric mucosal epithelial cell. We examined whether the miR-194 regulates cell migration and invasion, and the epithelial–mesenchymal transition Phenotype by inhibiting FoxM1 in gastric cancer cells.
Results
The expression of miR-194 was significantly lower in gastric cancer compared with non-cancerous gastric tissues and cells. Exogenous expression of miR-194 inhibited cell migration, invasion, and the epithelial–mesenchymal transition phenotype in gastric cancer cells. Moreover, we discovered a novel post-transcriptional regulatory mechanism of FoxM1 expression that is mediated by miR-194.
Conclusion
Our study clearly demonstrates that miR-194 inhibits the acquisition of the EMT phenotype in gastric cancer cells by downregulating FoxM1, thereby inhibiting cell migration and invasion during cancer progression. |
doi_str_mv | 10.1007/s10620-014-3159-6 |
format | article |
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We hypothesized that miR-194 may control Forkhead box protein M1 (FoxM1) expression in gastric cancer cells and therefore may have therapeutic potential in gastric cancer.
Methods
The expression level of miR-194 was examined using real-time PCR in human gastric cancer and noncancerous gastric tissues, gastric cancer cell and normal gastric mucosal epithelial cell. We examined whether the miR-194 regulates cell migration and invasion, and the epithelial–mesenchymal transition Phenotype by inhibiting FoxM1 in gastric cancer cells.
Results
The expression of miR-194 was significantly lower in gastric cancer compared with non-cancerous gastric tissues and cells. Exogenous expression of miR-194 inhibited cell migration, invasion, and the epithelial–mesenchymal transition phenotype in gastric cancer cells. Moreover, we discovered a novel post-transcriptional regulatory mechanism of FoxM1 expression that is mediated by miR-194.
Conclusion
Our study clearly demonstrates that miR-194 inhibits the acquisition of the EMT phenotype in gastric cancer cells by downregulating FoxM1, thereby inhibiting cell migration and invasion during cancer progression.</description><identifier>ISSN: 0163-2116</identifier><identifier>EISSN: 1573-2568</identifier><identifier>DOI: 10.1007/s10620-014-3159-6</identifier><identifier>PMID: 24748184</identifier><identifier>CODEN: DDSCDJ</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Biochemistry ; Cancer ; Cancer cells ; Cell Line, Tumor ; Cell Movement ; Comparative analysis ; Development and progression ; Epithelial Cells ; Epithelial-Mesenchymal Transition - genetics ; Forkhead Box Protein M1 ; Forkhead Transcription Factors - genetics ; Forkhead Transcription Factors - metabolism ; Gastric Mucosa - metabolism ; Gastroenterology ; Gene Expression Regulation, Neoplastic ; Health aspects ; Hepatology ; Humans ; Medicine ; Medicine & Public Health ; MicroRNA ; MicroRNAs - genetics ; MicroRNAs - metabolism ; MicroRNAs - physiology ; Oncology ; Original Article ; Phenotype ; RNA Interference ; Stem cells ; Stomach cancer ; Stomach Neoplasms - genetics ; Stomach Neoplasms - metabolism ; Transplant Surgery ; Up-Regulation</subject><ispartof>Digestive diseases and sciences, 2014-09, Vol.59 (9), p.2145-2152</ispartof><rights>Springer Science+Business Media New York 2014</rights><rights>COPYRIGHT 2014 Springer</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c505t-d0705307e1aec57785e76a836a1d270c35483a513ec4c0b5658614a36cdf94373</citedby><cites>FETCH-LOGICAL-c505t-d0705307e1aec57785e76a836a1d270c35483a513ec4c0b5658614a36cdf94373</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24748184$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Zhenjun</creatorcontrib><creatorcontrib>Ying, Xiaojiang</creatorcontrib><creatorcontrib>Chen, Hongliang</creatorcontrib><creatorcontrib>Ye, Pingjiang</creatorcontrib><creatorcontrib>Shen, Yi</creatorcontrib><creatorcontrib>Pan, Weihuo</creatorcontrib><creatorcontrib>Zhang, Lihua</creatorcontrib><title>MicroRNA-194 Inhibits the Epithelial–Mesenchymal Transition in Gastric Cancer Cells by Targeting FoxM1</title><title>Digestive diseases and sciences</title><addtitle>Dig Dis Sci</addtitle><addtitle>Dig Dis Sci</addtitle><description>Aim
We hypothesized that miR-194 may control Forkhead box protein M1 (FoxM1) expression in gastric cancer cells and therefore may have therapeutic potential in gastric cancer.
Methods
The expression level of miR-194 was examined using real-time PCR in human gastric cancer and noncancerous gastric tissues, gastric cancer cell and normal gastric mucosal epithelial cell. We examined whether the miR-194 regulates cell migration and invasion, and the epithelial–mesenchymal transition Phenotype by inhibiting FoxM1 in gastric cancer cells.
Results
The expression of miR-194 was significantly lower in gastric cancer compared with non-cancerous gastric tissues and cells. Exogenous expression of miR-194 inhibited cell migration, invasion, and the epithelial–mesenchymal transition phenotype in gastric cancer cells. Moreover, we discovered a novel post-transcriptional regulatory mechanism of FoxM1 expression that is mediated by miR-194.
Conclusion
Our study clearly demonstrates that miR-194 inhibits the acquisition of the EMT phenotype in gastric cancer cells by downregulating FoxM1, thereby inhibiting cell migration and invasion during cancer progression.</description><subject>Biochemistry</subject><subject>Cancer</subject><subject>Cancer cells</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Comparative analysis</subject><subject>Development and progression</subject><subject>Epithelial Cells</subject><subject>Epithelial-Mesenchymal Transition - genetics</subject><subject>Forkhead Box Protein M1</subject><subject>Forkhead Transcription Factors - genetics</subject><subject>Forkhead Transcription Factors - metabolism</subject><subject>Gastric Mucosa - metabolism</subject><subject>Gastroenterology</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Health aspects</subject><subject>Hepatology</subject><subject>Humans</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>MicroRNA</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>MicroRNAs - physiology</subject><subject>Oncology</subject><subject>Original Article</subject><subject>Phenotype</subject><subject>RNA Interference</subject><subject>Stem cells</subject><subject>Stomach cancer</subject><subject>Stomach Neoplasms - genetics</subject><subject>Stomach Neoplasms - metabolism</subject><subject>Transplant Surgery</subject><subject>Up-Regulation</subject><issn>0163-2116</issn><issn>1573-2568</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><recordid>eNqNks1uEzEQxy0EoqHwAFyQJS69bPGsv3aPUdSWSg2VUDhbjnc2cbXrDfZGIjfeoW_Ik-BVyqdAqnwYy_79xzOePyGvgZ0DY_pdAqZKVjAQBQdZF-oJmYHUvCilqp6SGQOV9wDqhLxI6Y4xVmtQz8lJKbSooBIzsl16F4ePH-YF1IJeh61f-zHRcYv0Yudz6Lztvn29X2LC4LaH3nZ0FW1IfvRDoD7QK5vG6B1d2OAw0gV2XaLrA13ZuMHRhw29HL4s4SV51tou4auHeEo-XV6sFu-Lm9ur68X8pnCSybFomGaSM41g0UmtK4la2YorC02pmeNSVNxK4OiEY2upZKVAWK5c09aCa35Kzo55d3H4vMc0mt4nl4uyAYd9MrnNsgRV6kegUlYyf6XmGX37F3o37GPIjUyUqnnFuPpFbWyHxod2GKN1U1Iz11Dml4WaqPN_UHk12Hs3BGx9Pv9DAEdBnlRKEVuzi7638WCAmckI5mgEk41gJiOYSfPmoeD9usfmp-LH5DNQHoGUr8IG428d_Tfrd_1yudg</recordid><startdate>20140901</startdate><enddate>20140901</enddate><creator>Li, Zhenjun</creator><creator>Ying, Xiaojiang</creator><creator>Chen, Hongliang</creator><creator>Ye, Pingjiang</creator><creator>Shen, Yi</creator><creator>Pan, Weihuo</creator><creator>Zhang, Lihua</creator><general>Springer US</general><general>Springer</general><general>Springer Nature B.V</general><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>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>7T5</scope><scope>H94</scope></search><sort><creationdate>20140901</creationdate><title>MicroRNA-194 Inhibits the Epithelial–Mesenchymal Transition in Gastric Cancer Cells by Targeting FoxM1</title><author>Li, Zhenjun ; Ying, Xiaojiang ; Chen, Hongliang ; Ye, Pingjiang ; Shen, Yi ; Pan, Weihuo ; Zhang, Lihua</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c505t-d0705307e1aec57785e76a836a1d270c35483a513ec4c0b5658614a36cdf94373</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Biochemistry</topic><topic>Cancer</topic><topic>Cancer cells</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement</topic><topic>Comparative analysis</topic><topic>Development and progression</topic><topic>Epithelial Cells</topic><topic>Epithelial-Mesenchymal Transition - genetics</topic><topic>Forkhead Box Protein M1</topic><topic>Forkhead Transcription Factors - genetics</topic><topic>Forkhead Transcription Factors - metabolism</topic><topic>Gastric Mucosa - metabolism</topic><topic>Gastroenterology</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Health aspects</topic><topic>Hepatology</topic><topic>Humans</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>MicroRNA</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>MicroRNAs - physiology</topic><topic>Oncology</topic><topic>Original Article</topic><topic>Phenotype</topic><topic>RNA Interference</topic><topic>Stem cells</topic><topic>Stomach cancer</topic><topic>Stomach Neoplasms - genetics</topic><topic>Stomach Neoplasms - metabolism</topic><topic>Transplant Surgery</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Zhenjun</creatorcontrib><creatorcontrib>Ying, Xiaojiang</creatorcontrib><creatorcontrib>Chen, Hongliang</creatorcontrib><creatorcontrib>Ye, Pingjiang</creatorcontrib><creatorcontrib>Shen, Yi</creatorcontrib><creatorcontrib>Pan, Weihuo</creatorcontrib><creatorcontrib>Zhang, Lihua</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database (ProQuest)</collection><collection>Health & Medical Collection (Proquest)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</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)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Family Health</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</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>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Digestive diseases and sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Zhenjun</au><au>Ying, Xiaojiang</au><au>Chen, Hongliang</au><au>Ye, Pingjiang</au><au>Shen, Yi</au><au>Pan, Weihuo</au><au>Zhang, Lihua</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MicroRNA-194 Inhibits the Epithelial–Mesenchymal Transition in Gastric Cancer Cells by Targeting FoxM1</atitle><jtitle>Digestive diseases and sciences</jtitle><stitle>Dig Dis Sci</stitle><addtitle>Dig Dis Sci</addtitle><date>2014-09-01</date><risdate>2014</risdate><volume>59</volume><issue>9</issue><spage>2145</spage><epage>2152</epage><pages>2145-2152</pages><issn>0163-2116</issn><eissn>1573-2568</eissn><coden>DDSCDJ</coden><abstract>Aim
We hypothesized that miR-194 may control Forkhead box protein M1 (FoxM1) expression in gastric cancer cells and therefore may have therapeutic potential in gastric cancer.
Methods
The expression level of miR-194 was examined using real-time PCR in human gastric cancer and noncancerous gastric tissues, gastric cancer cell and normal gastric mucosal epithelial cell. We examined whether the miR-194 regulates cell migration and invasion, and the epithelial–mesenchymal transition Phenotype by inhibiting FoxM1 in gastric cancer cells.
Results
The expression of miR-194 was significantly lower in gastric cancer compared with non-cancerous gastric tissues and cells. Exogenous expression of miR-194 inhibited cell migration, invasion, and the epithelial–mesenchymal transition phenotype in gastric cancer cells. Moreover, we discovered a novel post-transcriptional regulatory mechanism of FoxM1 expression that is mediated by miR-194.
Conclusion
Our study clearly demonstrates that miR-194 inhibits the acquisition of the EMT phenotype in gastric cancer cells by downregulating FoxM1, thereby inhibiting cell migration and invasion during cancer progression.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>24748184</pmid><doi>10.1007/s10620-014-3159-6</doi><tpages>8</tpages></addata></record> |
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subjects | Biochemistry Cancer Cancer cells Cell Line, Tumor Cell Movement Comparative analysis Development and progression Epithelial Cells Epithelial-Mesenchymal Transition - genetics Forkhead Box Protein M1 Forkhead Transcription Factors - genetics Forkhead Transcription Factors - metabolism Gastric Mucosa - metabolism Gastroenterology Gene Expression Regulation, Neoplastic Health aspects Hepatology Humans Medicine Medicine & Public Health MicroRNA MicroRNAs - genetics MicroRNAs - metabolism MicroRNAs - physiology Oncology Original Article Phenotype RNA Interference Stem cells Stomach cancer Stomach Neoplasms - genetics Stomach Neoplasms - metabolism Transplant Surgery Up-Regulation |
title | MicroRNA-194 Inhibits the Epithelial–Mesenchymal Transition in Gastric Cancer Cells by Targeting FoxM1 |
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