microRNA-181 promotes prostate cancer cell proliferation by regulating DAX-1 expression
microRNAs (miRNAs) are a class of short noncoding RNA molecules that have a critical role in the initiation and progression of types of human cancer, including prostate cancer. In the present study, the expression of miR-181 in prostate cancer tissues was evaluated and was demonstrated to be signifi...
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Veröffentlicht in: | Experimental and therapeutic medicine 2014-10, Vol.8 (4), p.1296-1300 |
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description | microRNAs (miRNAs) are a class of short noncoding RNA molecules that have a critical role in the initiation and progression of types of human cancer, including prostate cancer. In the present study, the expression of miR-181 in prostate cancer tissues was evaluated and was demonstrated to be significantly upregulated in prostate cancer tissues compared with that in adjacent normal tissues. The results of in vitro MTT and BrdU incorporation assays, as well as cell-cycle analysis, indicated that miR-181 overexpression markedly promoted the proliferation of LNCaP cells. Furthermore, miR-181 overexpression was found to promote the progression of LNCaP tumor growth in nude mice. Mechanistic studies demonstrated that dosage-sensitive sex reversal, adrenal hypoplasia critical region, on chromosome X, gene 1 (DAX-1), a negative regulator of androgen receptor in prostate cancer, was inhibited by miR-181 overexpression. Therefore, the results from the present study suggest that miR-181 functions as a growth-suppressive miRNA during prostate cancer development. |
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In the present study, the expression of miR-181 in prostate cancer tissues was evaluated and was demonstrated to be significantly upregulated in prostate cancer tissues compared with that in adjacent normal tissues. The results of in vitro MTT and BrdU incorporation assays, as well as cell-cycle analysis, indicated that miR-181 overexpression markedly promoted the proliferation of LNCaP cells. Furthermore, miR-181 overexpression was found to promote the progression of LNCaP tumor growth in nude mice. Mechanistic studies demonstrated that dosage-sensitive sex reversal, adrenal hypoplasia critical region, on chromosome X, gene 1 (DAX-1), a negative regulator of androgen receptor in prostate cancer, was inhibited by miR-181 overexpression. Therefore, the results from the present study suggest that miR-181 functions as a growth-suppressive miRNA during prostate cancer development.</description><identifier>ISSN: 1792-0981</identifier><identifier>EISSN: 1792-1015</identifier><identifier>DOI: 10.3892/etm.2014.1846</identifier><identifier>PMID: 25187843</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Androgens ; Cell growth ; Cell proliferation ; DAX-1 ; Development and progression ; Gene expression ; Genetic aspects ; Kinases ; MicroRNA ; miR-181 ; Physiological aspects ; Prostate cancer</subject><ispartof>Experimental and therapeutic medicine, 2014-10, Vol.8 (4), p.1296-1300</ispartof><rights>Copyright © 2014, Spandidos Publications</rights><rights>COPYRIGHT 2014 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2014</rights><rights>Copyright © 2014, Spandidos Publications 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c514t-7e602d812595db371f03fd4f08893be92a4c6abd6d1af20f5d906bb7d3eaded63</citedby><cites>FETCH-LOGICAL-c514t-7e602d812595db371f03fd4f08893be92a4c6abd6d1af20f5d906bb7d3eaded63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4151665/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4151665/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25187843$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>TONG, SHI-JUN</creatorcontrib><creatorcontrib>LIU, JUN</creatorcontrib><creatorcontrib>WANG, XIANG</creatorcontrib><creatorcontrib>QU, LIAN-XI</creatorcontrib><title>microRNA-181 promotes prostate cancer cell proliferation by regulating DAX-1 expression</title><title>Experimental and therapeutic medicine</title><addtitle>Exp Ther Med</addtitle><description>microRNAs (miRNAs) are a class of short noncoding RNA molecules that have a critical role in the initiation and progression of types of human cancer, including prostate cancer. In the present study, the expression of miR-181 in prostate cancer tissues was evaluated and was demonstrated to be significantly upregulated in prostate cancer tissues compared with that in adjacent normal tissues. The results of in vitro MTT and BrdU incorporation assays, as well as cell-cycle analysis, indicated that miR-181 overexpression markedly promoted the proliferation of LNCaP cells. Furthermore, miR-181 overexpression was found to promote the progression of LNCaP tumor growth in nude mice. Mechanistic studies demonstrated that dosage-sensitive sex reversal, adrenal hypoplasia critical region, on chromosome X, gene 1 (DAX-1), a negative regulator of androgen receptor in prostate cancer, was inhibited by miR-181 overexpression. Therefore, the results from the present study suggest that miR-181 functions as a growth-suppressive miRNA during prostate cancer development.</description><subject>Androgens</subject><subject>Cell growth</subject><subject>Cell proliferation</subject><subject>DAX-1</subject><subject>Development and progression</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Kinases</subject><subject>MicroRNA</subject><subject>miR-181</subject><subject>Physiological aspects</subject><subject>Prostate cancer</subject><issn>1792-0981</issn><issn>1792-1015</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptksGP1SAQxhujcTfrHr2aJh700icDhcLF5GXXVZONJkajN0LL8GTTlgqtcf_7pXnPp2uEAzDz4yPDfEXxFMiGSUVf4TxsKIF6A7IWD4pTaBStgAB_eNgTJeGkOE_phuTBBUjJHxcnlINsZM1Oi6-D72L49GFbgYRyimEIM6Z1k2YzY9mZscNYdtj3a7D3DqOZfRjL9raMuFv6fBp35eX2WwUl_poippTTT4pHzvQJzw_rWfHl6s3ni3fV9ce37y-211XHoZ6rBgWhVgLlituWNeAIc7Z2RErFWlTU1J0wrRUWjKPEcauIaNvGMjQWrWBnxeu97rS0A9oOxzmaXk_RDybe6mC8vp8Z_Xe9Cz91DRyE4Fng5UEghh8LplkPPq3lmhHDkjRIKgRhVK3o83_Qm7DEMZenQbH87U1D1B9qZ3rUfnQhv9utonrLVH6UU1FnavMfKk-LuSNhROdz_N6Fan8htyuliO5YIxC9mkFnM-jVDHo1Q-af_f0xR_p36zPwYg-kyYzW25COTFaqiKxIXQFVgt0Be9y75g</recordid><startdate>20141001</startdate><enddate>20141001</enddate><creator>TONG, SHI-JUN</creator><creator>LIU, JUN</creator><creator>WANG, XIANG</creator><creator>QU, LIAN-XI</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</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>KB0</scope><scope>M0S</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20141001</creationdate><title>microRNA-181 promotes prostate cancer cell proliferation by regulating DAX-1 expression</title><author>TONG, SHI-JUN ; LIU, JUN ; WANG, XIANG ; QU, LIAN-XI</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c514t-7e602d812595db371f03fd4f08893be92a4c6abd6d1af20f5d906bb7d3eaded63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Androgens</topic><topic>Cell growth</topic><topic>Cell proliferation</topic><topic>DAX-1</topic><topic>Development and progression</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><topic>Kinases</topic><topic>MicroRNA</topic><topic>miR-181</topic><topic>Physiological aspects</topic><topic>Prostate cancer</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>TONG, SHI-JUN</creatorcontrib><creatorcontrib>LIU, JUN</creatorcontrib><creatorcontrib>WANG, XIANG</creatorcontrib><creatorcontrib>QU, LIAN-XI</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</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>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</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>PubMed Central (Full Participant titles)</collection><jtitle>Experimental and therapeutic medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>TONG, SHI-JUN</au><au>LIU, JUN</au><au>WANG, XIANG</au><au>QU, LIAN-XI</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>microRNA-181 promotes prostate cancer cell proliferation by regulating DAX-1 expression</atitle><jtitle>Experimental and therapeutic medicine</jtitle><addtitle>Exp Ther Med</addtitle><date>2014-10-01</date><risdate>2014</risdate><volume>8</volume><issue>4</issue><spage>1296</spage><epage>1300</epage><pages>1296-1300</pages><issn>1792-0981</issn><eissn>1792-1015</eissn><abstract>microRNAs (miRNAs) are a class of short noncoding RNA molecules that have a critical role in the initiation and progression of types of human cancer, including prostate cancer. In the present study, the expression of miR-181 in prostate cancer tissues was evaluated and was demonstrated to be significantly upregulated in prostate cancer tissues compared with that in adjacent normal tissues. The results of in vitro MTT and BrdU incorporation assays, as well as cell-cycle analysis, indicated that miR-181 overexpression markedly promoted the proliferation of LNCaP cells. Furthermore, miR-181 overexpression was found to promote the progression of LNCaP tumor growth in nude mice. Mechanistic studies demonstrated that dosage-sensitive sex reversal, adrenal hypoplasia critical region, on chromosome X, gene 1 (DAX-1), a negative regulator of androgen receptor in prostate cancer, was inhibited by miR-181 overexpression. Therefore, the results from the present study suggest that miR-181 functions as a growth-suppressive miRNA during prostate cancer development.</abstract><cop>Greece</cop><pub>D.A. 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subjects | Androgens Cell growth Cell proliferation DAX-1 Development and progression Gene expression Genetic aspects Kinases MicroRNA miR-181 Physiological aspects Prostate cancer |
title | microRNA-181 promotes prostate cancer cell proliferation by regulating DAX-1 expression |
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