Upregulation of Limk1 caused by microRNA-138 loss aggravates the metastasis of ovarian cancer by activation of Limk1/cofilin signaling
LIM kinase 1 (Limk1) is associated with cell proliferation and metastasis and its dysregulated expression has been observed in many types of cancer. The present study aimed to examine the role of Limk1 in the development of ovarian cancer, as well as the underlying molecular mechanism involved. The...
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| Veröffentlicht in: | Oncology reports 2014-11, Vol.32 (5), p.2070-2076 |
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| creator | CHEN, PUXIANG ZENG, MENGJUN ZHAO, YAN FANG, XIAOLIN |
| description | LIM kinase 1 (Limk1) is associated with cell proliferation and metastasis and its dysregulated expression has been observed in many types of cancer. The present study aimed to examine the role of Limk1 in the development of ovarian cancer, as well as the underlying molecular mechanism involved. The results showed that increased Limk1 and decreased miR-138 expression co-existed in ovarian cancer. Furthermore, knockout of Limk1 or the overexpression of miR-138 resulted in reduced cell invasion and migration, while silencing of miR-138 led to enhancement of the invasion and migration of ovarian cancer cells. Cell growth was inhibited by the overexpression of miR-138, although not by the knockout of Limk1. miR-138 directly targeted Limk1 and inhibited ovarian cancer cell growth by PCNA and Bcl-2. Moreover, Limk1/cofilin/p-cofilin is likely a critical signaling pathway involving in miR-138 modulation of ovarian cancer cell metastasis. The results provide evidence supporting miR-138/Limk1 as a novel diagnostic or therapeutic target for ovarian cancer. |
| doi_str_mv | 10.3892/or.2014.3461 |
| format | Article |
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The present study aimed to examine the role of Limk1 in the development of ovarian cancer, as well as the underlying molecular mechanism involved. The results showed that increased Limk1 and decreased miR-138 expression co-existed in ovarian cancer. Furthermore, knockout of Limk1 or the overexpression of miR-138 resulted in reduced cell invasion and migration, while silencing of miR-138 led to enhancement of the invasion and migration of ovarian cancer cells. Cell growth was inhibited by the overexpression of miR-138, although not by the knockout of Limk1. miR-138 directly targeted Limk1 and inhibited ovarian cancer cell growth by PCNA and Bcl-2. Moreover, Limk1/cofilin/p-cofilin is likely a critical signaling pathway involving in miR-138 modulation of ovarian cancer cell metastasis. The results provide evidence supporting miR-138/Limk1 as a novel diagnostic or therapeutic target for ovarian cancer.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.2014.3461</identifier><identifier>PMID: 25190487</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Actin Depolymerizing Factors - genetics ; Actin Depolymerizing Factors - metabolism ; Apoptosis ; Cancer ; Cancer therapies ; Cell cycle ; Cell growth ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; cofilin ; Colorectal cancer ; Female ; Gene expression ; Gene Expression Regulation, Neoplastic ; Gene Knockout Techniques ; Genetic aspects ; Humans ; Kinases ; LIM kinase 1 ; Lim Kinases - genetics ; Lim Kinases - metabolism ; Lung cancer ; Metastasis ; MicroRNA ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miR-138 ; Neoplasm Metastasis ; Oncology, Experimental ; Ovarian cancer ; Ovarian Neoplasms - genetics ; Ovarian Neoplasms - metabolism ; Ovarian Neoplasms - pathology ; Physiological aspects ; Proteins ; Signal Transduction ; Software ; Talen technology ; Tumors</subject><ispartof>Oncology reports, 2014-11, Vol.32 (5), p.2070-2076</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-c552t-1e59ba6604e3076132ec13f35b21a1d818e6d279f4dfa677994d6d2ef6eca4dd3</citedby><cites>FETCH-LOGICAL-c552t-1e59ba6604e3076132ec13f35b21a1d818e6d279f4dfa677994d6d2ef6eca4dd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25190487$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>CHEN, PUXIANG</creatorcontrib><creatorcontrib>ZENG, MENGJUN</creatorcontrib><creatorcontrib>ZHAO, YAN</creatorcontrib><creatorcontrib>FANG, XIAOLIN</creatorcontrib><title>Upregulation of Limk1 caused by microRNA-138 loss aggravates the metastasis of ovarian cancer by activation of Limk1/cofilin signaling</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>LIM kinase 1 (Limk1) is associated with cell proliferation and metastasis and its dysregulated expression has been observed in many types of cancer. The present study aimed to examine the role of Limk1 in the development of ovarian cancer, as well as the underlying molecular mechanism involved. The results showed that increased Limk1 and decreased miR-138 expression co-existed in ovarian cancer. Furthermore, knockout of Limk1 or the overexpression of miR-138 resulted in reduced cell invasion and migration, while silencing of miR-138 led to enhancement of the invasion and migration of ovarian cancer cells. Cell growth was inhibited by the overexpression of miR-138, although not by the knockout of Limk1. miR-138 directly targeted Limk1 and inhibited ovarian cancer cell growth by PCNA and Bcl-2. Moreover, Limk1/cofilin/p-cofilin is likely a critical signaling pathway involving in miR-138 modulation of ovarian cancer cell metastasis. The results provide evidence supporting miR-138/Limk1 as a novel diagnostic or therapeutic target for ovarian cancer.</description><subject>Actin Depolymerizing Factors - genetics</subject><subject>Actin Depolymerizing Factors - metabolism</subject><subject>Apoptosis</subject><subject>Cancer</subject><subject>Cancer therapies</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>cofilin</subject><subject>Colorectal cancer</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene Knockout Techniques</subject><subject>Genetic aspects</subject><subject>Humans</subject><subject>Kinases</subject><subject>LIM kinase 1</subject><subject>Lim Kinases - genetics</subject><subject>Lim Kinases - metabolism</subject><subject>Lung cancer</subject><subject>Metastasis</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miR-138</subject><subject>Neoplasm Metastasis</subject><subject>Oncology, Experimental</subject><subject>Ovarian cancer</subject><subject>Ovarian Neoplasms - genetics</subject><subject>Ovarian Neoplasms - metabolism</subject><subject>Ovarian Neoplasms - pathology</subject><subject>Physiological aspects</subject><subject>Proteins</subject><subject>Signal Transduction</subject><subject>Software</subject><subject>Talen technology</subject><subject>Tumors</subject><issn>1021-335X</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptkl1rFDEUhoMotlbvvJaAULxwtvmaj1wuxS9YFMSCd-FscmY2dWayJjML_QP-bjO0tq5IAjmE57xJ3ryEvORsJRstLkJcCcbVSqqKPyKnvNa8EEryx7lmghdSlt9PyLOUrhkTNav0U3IiSq6ZaupT8utqH7Gbe5h8GGlo6cYPPzi1MCd0dHtDB29j-Pp5XXDZ0D6kRKHrIhxgwkSnHdIBJ0h5-rS0hwNED2MWGC3GRQDs5A_H8hc2tL73I02-GyEX3XPypIU-4Yu79YxcvX_37fJjsfny4dPlelPYshRTwbHUW6gqplCyuuJSoOWyleVWcOCu4Q1WTtS6Va6Fqq61Vi5vYFuhBeWcPCNvbnX3MfycMU1m8Mli38OIYU6GZ02tFJMio6__Qa_DHPN1M6WlqGopuXygOujR-LENUwS7iJp1VtK6YXKhVv-h8nCY_Q0jZjvwuOH8r4YdQj_tUujnxcZ0DL69BfMvpRSxNfvoB4g3hjOz5MOEaJZ8mCUfGX9196h5O6C7h_8E4uHgtIfReRfSPRNiIUXBykKwmsnfBSDAKw</recordid><startdate>20141101</startdate><enddate>20141101</enddate><creator>CHEN, PUXIANG</creator><creator>ZENG, MENGJUN</creator><creator>ZHAO, YAN</creator><creator>FANG, XIAOLIN</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20141101</creationdate><title>Upregulation of Limk1 caused by microRNA-138 loss aggravates the metastasis of ovarian cancer by activation of Limk1/cofilin signaling</title><author>CHEN, PUXIANG ; ZENG, MENGJUN ; ZHAO, YAN ; FANG, XIAOLIN</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c552t-1e59ba6604e3076132ec13f35b21a1d818e6d279f4dfa677994d6d2ef6eca4dd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Actin Depolymerizing Factors - genetics</topic><topic>Actin Depolymerizing Factors - metabolism</topic><topic>Apoptosis</topic><topic>Cancer</topic><topic>Cancer therapies</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>cofilin</topic><topic>Colorectal cancer</topic><topic>Female</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene Knockout Techniques</topic><topic>Genetic aspects</topic><topic>Humans</topic><topic>Kinases</topic><topic>LIM kinase 1</topic><topic>Lim Kinases - genetics</topic><topic>Lim Kinases - metabolism</topic><topic>Lung cancer</topic><topic>Metastasis</topic><topic>MicroRNA</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miR-138</topic><topic>Neoplasm Metastasis</topic><topic>Oncology, Experimental</topic><topic>Ovarian cancer</topic><topic>Ovarian Neoplasms - genetics</topic><topic>Ovarian Neoplasms - metabolism</topic><topic>Ovarian Neoplasms - pathology</topic><topic>Physiological aspects</topic><topic>Proteins</topic><topic>Signal Transduction</topic><topic>Software</topic><topic>Talen technology</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>CHEN, PUXIANG</creatorcontrib><creatorcontrib>ZENG, MENGJUN</creatorcontrib><creatorcontrib>ZHAO, YAN</creatorcontrib><creatorcontrib>FANG, XIAOLIN</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</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><jtitle>Oncology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>CHEN, PUXIANG</au><au>ZENG, MENGJUN</au><au>ZHAO, YAN</au><au>FANG, XIAOLIN</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Upregulation of Limk1 caused by microRNA-138 loss aggravates the metastasis of ovarian cancer by activation of Limk1/cofilin signaling</atitle><jtitle>Oncology reports</jtitle><addtitle>Oncol Rep</addtitle><date>2014-11-01</date><risdate>2014</risdate><volume>32</volume><issue>5</issue><spage>2070</spage><epage>2076</epage><pages>2070-2076</pages><issn>1021-335X</issn><eissn>1791-2431</eissn><abstract>LIM kinase 1 (Limk1) is associated with cell proliferation and metastasis and its dysregulated expression has been observed in many types of cancer. The present study aimed to examine the role of Limk1 in the development of ovarian cancer, as well as the underlying molecular mechanism involved. The results showed that increased Limk1 and decreased miR-138 expression co-existed in ovarian cancer. Furthermore, knockout of Limk1 or the overexpression of miR-138 resulted in reduced cell invasion and migration, while silencing of miR-138 led to enhancement of the invasion and migration of ovarian cancer cells. Cell growth was inhibited by the overexpression of miR-138, although not by the knockout of Limk1. miR-138 directly targeted Limk1 and inhibited ovarian cancer cell growth by PCNA and Bcl-2. Moreover, Limk1/cofilin/p-cofilin is likely a critical signaling pathway involving in miR-138 modulation of ovarian cancer cell metastasis. The results provide evidence supporting miR-138/Limk1 as a novel diagnostic or therapeutic target for ovarian cancer.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>25190487</pmid><doi>10.3892/or.2014.3461</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Actin Depolymerizing Factors - genetics Actin Depolymerizing Factors - metabolism Apoptosis Cancer Cancer therapies Cell cycle Cell growth Cell Line, Tumor Cell Movement Cell Proliferation cofilin Colorectal cancer Female Gene expression Gene Expression Regulation, Neoplastic Gene Knockout Techniques Genetic aspects Humans Kinases LIM kinase 1 Lim Kinases - genetics Lim Kinases - metabolism Lung cancer Metastasis MicroRNA MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism miR-138 Neoplasm Metastasis Oncology, Experimental Ovarian cancer Ovarian Neoplasms - genetics Ovarian Neoplasms - metabolism Ovarian Neoplasms - pathology Physiological aspects Proteins Signal Transduction Software Talen technology Tumors |
| title | Upregulation of Limk1 caused by microRNA-138 loss aggravates the metastasis of ovarian cancer by activation of Limk1/cofilin signaling |
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