MicroRNA-185 suppresses proliferation, invasion, migration, and tumorigenicity of human prostate cancer cells through targeting androgen receptor
Previous studies have shown that androgen receptor (AR) is involved in the progression of prostate cancer (CaP) by several mechanisms. However, how AR is regulated has not been fully understood. In this study, miR-185 was found to be down-regulated in clinical CaP samples. Targets prediction reveale...
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| Veröffentlicht in: | Molecular and cellular biochemistry 2013-05, Vol.377 (1-2), p.121-130 |
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| container_title | Molecular and cellular biochemistry |
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| creator | Qu, Fajun Cui, Xingang Hong, Yi Wang, Junkai Li, Yao Chen, Lu Liu, Yushan Gao, Yi Xu, Danfeng Wang, Quanxing |
| description | Previous studies have shown that androgen receptor (AR) is involved in the progression of prostate cancer (CaP) by several mechanisms. However, how AR is regulated has not been fully understood. In this study, miR-185 was found to be down-regulated in clinical CaP samples. Targets prediction revealed that AR had putative complementary sequences to miR-185, which was confirmed by the following dual luciferase reporter assay. Overexpression of miR-185 could reduce the expression of AR protein but not mRNA in LNCaP cells. The proliferation of LNCaP cells was inhibited by overexpression of miR-185. Cell cycle analysis revealed cell cycle arrest at G0/G1 phase. The invasive and migration abilities of cells could also be suppressed by miR-185. Furthermore, miR-185 inhibited tumorigenicity in a CaP xenografts model. CDC6, one target of AR and an important regulatory molecule for cell cycle, was found to be down-regulated by overexpression of miR-185. Our findings suggest that miR-185 could function as a tumor-suppressor gene in CaP by directly targeting AR, and act as a potential therapeutic target for CaP. |
| doi_str_mv | 10.1007/s11010-013-1576-z |
| format | Article |
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However, how AR is regulated has not been fully understood. In this study, miR-185 was found to be down-regulated in clinical CaP samples. Targets prediction revealed that AR had putative complementary sequences to miR-185, which was confirmed by the following dual luciferase reporter assay. Overexpression of miR-185 could reduce the expression of AR protein but not mRNA in LNCaP cells. The proliferation of LNCaP cells was inhibited by overexpression of miR-185. Cell cycle analysis revealed cell cycle arrest at G0/G1 phase. The invasive and migration abilities of cells could also be suppressed by miR-185. Furthermore, miR-185 inhibited tumorigenicity in a CaP xenografts model. CDC6, one target of AR and an important regulatory molecule for cell cycle, was found to be down-regulated by overexpression of miR-185. Our findings suggest that miR-185 could function as a tumor-suppressor gene in CaP by directly targeting AR, and act as a potential therapeutic target for CaP.</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/s11010-013-1576-z</identifier><identifier>PMID: 23417242</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Analysis ; Androgens ; Animals ; Base Sequence ; Binding Sites ; Biochemistry ; Biomedical and Life Sciences ; Cardiology ; Cell adhesion & migration ; Cell Cycle Proteins - genetics ; Cell Cycle Proteins - metabolism ; Cell growth ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Cell Transformation, Neoplastic - metabolism ; Development and progression ; G1 Phase Cell Cycle Checkpoints ; Gene Expression ; Gene Expression Regulation, Neoplastic ; Health aspects ; HEK293 Cells ; Humans ; Life Sciences ; Luciferase ; Male ; Medical Biochemistry ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; MicroRNA ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Neoplasm Invasiveness ; Neoplasm Transplantation ; Nuclear Proteins - genetics ; Nuclear Proteins - metabolism ; Oncology ; Prostate cancer ; Prostatic Neoplasms - metabolism ; Prostatic Neoplasms - pathology ; Receptors, Androgen - genetics ; Receptors, Androgen - metabolism ; Ribonucleic acid ; RNA ; RNA Interference ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Tumor Burden</subject><ispartof>Molecular and cellular biochemistry, 2013-05, Vol.377 (1-2), p.121-130</ispartof><rights>Springer Science+Business Media New York 2013</rights><rights>COPYRIGHT 2013 Springer</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c539t-a0bb5accdc1a272a9b1e288513956d787ce811b435f1eb2f9f3b030cdbbe3b763</citedby><cites>FETCH-LOGICAL-c539t-a0bb5accdc1a272a9b1e288513956d787ce811b435f1eb2f9f3b030cdbbe3b763</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11010-013-1576-z$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11010-013-1576-z$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,777,781,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23417242$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Qu, Fajun</creatorcontrib><creatorcontrib>Cui, Xingang</creatorcontrib><creatorcontrib>Hong, Yi</creatorcontrib><creatorcontrib>Wang, Junkai</creatorcontrib><creatorcontrib>Li, Yao</creatorcontrib><creatorcontrib>Chen, Lu</creatorcontrib><creatorcontrib>Liu, Yushan</creatorcontrib><creatorcontrib>Gao, Yi</creatorcontrib><creatorcontrib>Xu, Danfeng</creatorcontrib><creatorcontrib>Wang, Quanxing</creatorcontrib><title>MicroRNA-185 suppresses proliferation, invasion, migration, and tumorigenicity of human prostate cancer cells through targeting androgen receptor</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><addtitle>Mol Cell Biochem</addtitle><description>Previous studies have shown that androgen receptor (AR) is involved in the progression of prostate cancer (CaP) by several mechanisms. However, how AR is regulated has not been fully understood. In this study, miR-185 was found to be down-regulated in clinical CaP samples. Targets prediction revealed that AR had putative complementary sequences to miR-185, which was confirmed by the following dual luciferase reporter assay. Overexpression of miR-185 could reduce the expression of AR protein but not mRNA in LNCaP cells. The proliferation of LNCaP cells was inhibited by overexpression of miR-185. Cell cycle analysis revealed cell cycle arrest at G0/G1 phase. The invasive and migration abilities of cells could also be suppressed by miR-185. Furthermore, miR-185 inhibited tumorigenicity in a CaP xenografts model. CDC6, one target of AR and an important regulatory molecule for cell cycle, was found to be down-regulated by overexpression of miR-185. Our findings suggest that miR-185 could function as a tumor-suppressor gene in CaP by directly targeting AR, and act as a potential therapeutic target for CaP.</description><subject>Analysis</subject><subject>Androgens</subject><subject>Animals</subject><subject>Base Sequence</subject><subject>Binding Sites</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cardiology</subject><subject>Cell adhesion & migration</subject><subject>Cell Cycle Proteins - genetics</subject><subject>Cell Cycle Proteins - metabolism</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Cell Transformation, Neoplastic - metabolism</subject><subject>Development and progression</subject><subject>G1 Phase Cell Cycle Checkpoints</subject><subject>Gene Expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Health aspects</subject><subject>HEK293 Cells</subject><subject>Humans</subject><subject>Life Sciences</subject><subject>Luciferase</subject><subject>Male</subject><subject>Medical Biochemistry</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>MicroRNA</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Neoplasm Invasiveness</subject><subject>Neoplasm Transplantation</subject><subject>Nuclear Proteins - genetics</subject><subject>Nuclear Proteins - metabolism</subject><subject>Oncology</subject><subject>Prostate cancer</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>Prostatic Neoplasms - pathology</subject><subject>Receptors, Androgen - genetics</subject><subject>Receptors, Androgen - metabolism</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA Interference</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Tumor Burden</subject><issn>0300-8177</issn><issn>1573-4919</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNUtGK1DAULaK44-oH-CIBX-2a2zRN-zgsuiusCqLPIUlvO1napCapsPsX_rEZZ1dGUJE85HJzzrnh3FMUz4GeAaXidQSgQEsKrAQumvL2QbHJBSvrDrqHxYYySssWhDgpnsR4TTOYAjwuTipWg6jqalN8f29N8J8-bEtoOYnrsgSMESNZgp_sgEEl690rYt03FX9Wsx3vm8r1JK2zD3ZEZ41NN8QPZLfOyu35MamExChnMBCD0xRJ2gW_jjuSVBgxWTfuNYLPdBLQ4JJ8eFo8GtQU8dndfVp8efvm8_llefXx4t359qo0nHWpVFRrrozpDahKVKrTgFXbcmAdb3rRCoMtgK4ZHwB1NXQD09kP02uNTIuGnRYvD7r5p19XjEle-zW4PFICa2reUDhGjWpCad3gU1BmttHIbV13XAjg_J8oxpq8AWCQUWd_QOXT42yNdzjY3P9N9r8IxxPgQMg7jTHgIJdgZxVuJFC5j4w8REbmyMh9ZORt5ry482HVM_a_GPcZyYDqAIj5yY0Yjoz6q-oP5bvMZA</recordid><startdate>20130501</startdate><enddate>20130501</enddate><creator>Qu, Fajun</creator><creator>Cui, Xingang</creator><creator>Hong, Yi</creator><creator>Wang, Junkai</creator><creator>Li, Yao</creator><creator>Chen, Lu</creator><creator>Liu, Yushan</creator><creator>Gao, Yi</creator><creator>Xu, Danfeng</creator><creator>Wang, Quanxing</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>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope></search><sort><creationdate>20130501</creationdate><title>MicroRNA-185 suppresses proliferation, invasion, migration, and tumorigenicity of human prostate cancer cells through targeting androgen receptor</title><author>Qu, Fajun ; Cui, Xingang ; Hong, Yi ; Wang, Junkai ; Li, Yao ; Chen, Lu ; Liu, Yushan ; Gao, Yi ; Xu, Danfeng ; Wang, Quanxing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c539t-a0bb5accdc1a272a9b1e288513956d787ce811b435f1eb2f9f3b030cdbbe3b763</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Analysis</topic><topic>Androgens</topic><topic>Animals</topic><topic>Base Sequence</topic><topic>Binding Sites</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Cardiology</topic><topic>Cell adhesion & migration</topic><topic>Cell Cycle Proteins - 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However, how AR is regulated has not been fully understood. In this study, miR-185 was found to be down-regulated in clinical CaP samples. Targets prediction revealed that AR had putative complementary sequences to miR-185, which was confirmed by the following dual luciferase reporter assay. Overexpression of miR-185 could reduce the expression of AR protein but not mRNA in LNCaP cells. The proliferation of LNCaP cells was inhibited by overexpression of miR-185. Cell cycle analysis revealed cell cycle arrest at G0/G1 phase. The invasive and migration abilities of cells could also be suppressed by miR-185. Furthermore, miR-185 inhibited tumorigenicity in a CaP xenografts model. CDC6, one target of AR and an important regulatory molecule for cell cycle, was found to be down-regulated by overexpression of miR-185. Our findings suggest that miR-185 could function as a tumor-suppressor gene in CaP by directly targeting AR, and act as a potential therapeutic target for CaP.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>23417242</pmid><doi>10.1007/s11010-013-1576-z</doi><tpages>10</tpages></addata></record> |
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| ispartof | Molecular and cellular biochemistry, 2013-05, Vol.377 (1-2), p.121-130 |
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| subjects | Analysis Androgens Animals Base Sequence Binding Sites Biochemistry Biomedical and Life Sciences Cardiology Cell adhesion & migration Cell Cycle Proteins - genetics Cell Cycle Proteins - metabolism Cell growth Cell Line, Tumor Cell Movement Cell Proliferation Cell Transformation, Neoplastic - metabolism Development and progression G1 Phase Cell Cycle Checkpoints Gene Expression Gene Expression Regulation, Neoplastic Health aspects HEK293 Cells Humans Life Sciences Luciferase Male Medical Biochemistry Mice Mice, Inbred BALB C Mice, Nude MicroRNA MicroRNAs - genetics MicroRNAs - metabolism Neoplasm Invasiveness Neoplasm Transplantation Nuclear Proteins - genetics Nuclear Proteins - metabolism Oncology Prostate cancer Prostatic Neoplasms - metabolism Prostatic Neoplasms - pathology Receptors, Androgen - genetics Receptors, Androgen - metabolism Ribonucleic acid RNA RNA Interference RNA, Messenger - genetics RNA, Messenger - metabolism Tumor Burden |
| title | MicroRNA-185 suppresses proliferation, invasion, migration, and tumorigenicity of human prostate cancer cells through targeting androgen receptor |
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