miR-154 inhibits prostate cancer cell proliferation by targeting CCND2
Abstract Background Research has shown reduced expression levels of miR-154 in prostate cancer (CaP). However, the function and molecular mechanisms of miR-154 in this cancer type remains unknown. Objective The aims of this study were to examine the functional significance of miR-154 in CaP cells an...
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| creator | Zhu, Chen, M.S Shao, Pengfei, M.D., Ph.D Bao, Meiling, M.S Li, Pu, M.S Zhou, Hai, M.S Cai, Hongzhou, M.S Cao, Qiang, M.S Tao, Liangjun, M.S Meng, Xiaoxin, M.D., Ph.D Ju, Xiaobing, M.D., Ph.D Qin, Chao, M.D., Ph.D Li, Jie, M.D., Ph.D Yin, Changjun, M.D., Ph.D |
| description | Abstract Background Research has shown reduced expression levels of miR-154 in prostate cancer (CaP). However, the function and molecular mechanisms of miR-154 in this cancer type remains unknown. Objective The aims of this study were to examine the functional significance of miR-154 in CaP cells and to identify the novel molecular targets regulated by miR-154. Materials and methods miR-154 expression significantly decreased in primary CaP samples compared with nonmalignant samples measured by quantitative reverse transcription polymerase chain reaction. Restoration of miR-154 lowered the potential of CaP cell lines to grow and proliferate in vitro evaluated by CCK-8 assay, colony formation assay, and flow cytometry. miR-154 down-regulated the expression of CCND2 by binding to its 3′-untranslated region by luciferase reporter assay. Conclusions miR-154 plays a prominent role in CaP proliferation by suppressing CCND2, and it may provide a new approach to the treatment of CaP. |
| doi_str_mv | 10.1016/j.urolonc.2012.11.013 |
| format | Article |
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However, the function and molecular mechanisms of miR-154 in this cancer type remains unknown. Objective The aims of this study were to examine the functional significance of miR-154 in CaP cells and to identify the novel molecular targets regulated by miR-154. Materials and methods miR-154 expression significantly decreased in primary CaP samples compared with nonmalignant samples measured by quantitative reverse transcription polymerase chain reaction. Restoration of miR-154 lowered the potential of CaP cell lines to grow and proliferate in vitro evaluated by CCK-8 assay, colony formation assay, and flow cytometry. miR-154 down-regulated the expression of CCND2 by binding to its 3′-untranslated region by luciferase reporter assay. Conclusions miR-154 plays a prominent role in CaP proliferation by suppressing CCND2, and it may provide a new approach to the treatment of CaP.</description><identifier>ISSN: 1078-1439</identifier><identifier>EISSN: 1873-2496</identifier><identifier>DOI: 10.1016/j.urolonc.2012.11.013</identifier><identifier>PMID: 23428540</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Aged ; CCND2 ; Cell Cycle ; Cell Enlargement ; Cell Line, Tumor ; Cell Proliferation ; Cyclin D2 - metabolism ; Gene Expression Regulation, Neoplastic ; Humans ; Male ; MicroRNAs - physiology ; Middle Aged ; miR-154 ; Prostate cancer ; Prostatic Neoplasms - genetics ; Prostatic Neoplasms - metabolism ; Urology</subject><ispartof>Urologic oncology, 2014, Vol.32 (1), p.31.e9-31.e16</ispartof><rights>2014</rights><rights>Copyright © 2014. Published by Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c420t-b114bf8c66568d79b3ee1cb76f6a434882d56a6ca3a89d22176a5c4f76290a423</citedby><cites>FETCH-LOGICAL-c420t-b114bf8c66568d79b3ee1cb76f6a434882d56a6ca3a89d22176a5c4f76290a423</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1078143912004061$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,4010,27900,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23428540$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhu, Chen, M.S</creatorcontrib><creatorcontrib>Shao, Pengfei, M.D., Ph.D</creatorcontrib><creatorcontrib>Bao, Meiling, M.S</creatorcontrib><creatorcontrib>Li, Pu, M.S</creatorcontrib><creatorcontrib>Zhou, Hai, M.S</creatorcontrib><creatorcontrib>Cai, Hongzhou, M.S</creatorcontrib><creatorcontrib>Cao, Qiang, M.S</creatorcontrib><creatorcontrib>Tao, Liangjun, M.S</creatorcontrib><creatorcontrib>Meng, Xiaoxin, M.D., Ph.D</creatorcontrib><creatorcontrib>Ju, Xiaobing, M.D., Ph.D</creatorcontrib><creatorcontrib>Qin, Chao, M.D., Ph.D</creatorcontrib><creatorcontrib>Li, Jie, M.D., Ph.D</creatorcontrib><creatorcontrib>Yin, Changjun, M.D., Ph.D</creatorcontrib><title>miR-154 inhibits prostate cancer cell proliferation by targeting CCND2</title><title>Urologic oncology</title><addtitle>Urol Oncol</addtitle><description>Abstract Background Research has shown reduced expression levels of miR-154 in prostate cancer (CaP). However, the function and molecular mechanisms of miR-154 in this cancer type remains unknown. Objective The aims of this study were to examine the functional significance of miR-154 in CaP cells and to identify the novel molecular targets regulated by miR-154. Materials and methods miR-154 expression significantly decreased in primary CaP samples compared with nonmalignant samples measured by quantitative reverse transcription polymerase chain reaction. Restoration of miR-154 lowered the potential of CaP cell lines to grow and proliferate in vitro evaluated by CCK-8 assay, colony formation assay, and flow cytometry. miR-154 down-regulated the expression of CCND2 by binding to its 3′-untranslated region by luciferase reporter assay. Conclusions miR-154 plays a prominent role in CaP proliferation by suppressing CCND2, and it may provide a new approach to the treatment of CaP.</description><subject>Aged</subject><subject>CCND2</subject><subject>Cell Cycle</subject><subject>Cell Enlargement</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Cyclin D2 - metabolism</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Male</subject><subject>MicroRNAs - physiology</subject><subject>Middle Aged</subject><subject>miR-154</subject><subject>Prostate cancer</subject><subject>Prostatic Neoplasms - genetics</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>Urology</subject><issn>1078-1439</issn><issn>1873-2496</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1P3DAQhi1EBZT2J1DlyCXBYzuOcwGhhYVKq1bqx9lynMnibTYB26m0_76OduHApacZjd75eJ8h5AJoARTk1aaY_NiPgy0YBVYAFBT4ETkDVfGciVoep5xWKgfB61PyMYQNpSAUwAk5ZVwwVQp6RpZb9yOHUmRueHKNiyF79mOIJmJmzWDRZxb7fi72rkNvohuHrNll0fg1Rjess8Xi2x37RD50pg_4-RDPye_l_a_FY776_vB1cbvKrWA05g2AaDplpSylaqu64Yhgm0p20ggulGJtKY20hhtVt4xBJU1pRVdJVlMjGD8nl_u56aCXCUPUWxfmC82A4xQ0iDp5hrKqkrTcS20yFDx2-tm7rfE7DVTPCPVGHxDqGaEG0Alh6vtyWDE1W2zful6ZJcHNXoDJ6F-HXgfrMLFqnUcbdTu6_664fjfB9m5w1vR_cIdhM05-SBQ16MA01T_nP85vBEapoBL4P57WmBo</recordid><startdate>2014</startdate><enddate>2014</enddate><creator>Zhu, Chen, M.S</creator><creator>Shao, Pengfei, M.D., Ph.D</creator><creator>Bao, Meiling, M.S</creator><creator>Li, Pu, M.S</creator><creator>Zhou, Hai, M.S</creator><creator>Cai, Hongzhou, M.S</creator><creator>Cao, Qiang, M.S</creator><creator>Tao, Liangjun, M.S</creator><creator>Meng, Xiaoxin, M.D., Ph.D</creator><creator>Ju, Xiaobing, M.D., Ph.D</creator><creator>Qin, Chao, M.D., Ph.D</creator><creator>Li, Jie, M.D., Ph.D</creator><creator>Yin, Changjun, M.D., Ph.D</creator><general>Elsevier Inc</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>7X8</scope></search><sort><creationdate>2014</creationdate><title>miR-154 inhibits prostate cancer cell proliferation by targeting CCND2</title><author>Zhu, Chen, M.S ; Shao, Pengfei, M.D., Ph.D ; Bao, Meiling, M.S ; Li, Pu, M.S ; Zhou, Hai, M.S ; Cai, Hongzhou, M.S ; Cao, Qiang, M.S ; Tao, Liangjun, M.S ; Meng, Xiaoxin, M.D., Ph.D ; Ju, Xiaobing, M.D., Ph.D ; Qin, Chao, M.D., Ph.D ; Li, Jie, M.D., Ph.D ; Yin, Changjun, M.D., Ph.D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c420t-b114bf8c66568d79b3ee1cb76f6a434882d56a6ca3a89d22176a5c4f76290a423</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Aged</topic><topic>CCND2</topic><topic>Cell Cycle</topic><topic>Cell Enlargement</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Cyclin D2 - metabolism</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Male</topic><topic>MicroRNAs - physiology</topic><topic>Middle Aged</topic><topic>miR-154</topic><topic>Prostate cancer</topic><topic>Prostatic Neoplasms - genetics</topic><topic>Prostatic Neoplasms - metabolism</topic><topic>Urology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhu, Chen, M.S</creatorcontrib><creatorcontrib>Shao, Pengfei, M.D., Ph.D</creatorcontrib><creatorcontrib>Bao, Meiling, M.S</creatorcontrib><creatorcontrib>Li, Pu, M.S</creatorcontrib><creatorcontrib>Zhou, Hai, M.S</creatorcontrib><creatorcontrib>Cai, Hongzhou, M.S</creatorcontrib><creatorcontrib>Cao, Qiang, M.S</creatorcontrib><creatorcontrib>Tao, Liangjun, M.S</creatorcontrib><creatorcontrib>Meng, Xiaoxin, M.D., Ph.D</creatorcontrib><creatorcontrib>Ju, Xiaobing, M.D., Ph.D</creatorcontrib><creatorcontrib>Qin, Chao, M.D., Ph.D</creatorcontrib><creatorcontrib>Li, Jie, M.D., Ph.D</creatorcontrib><creatorcontrib>Yin, Changjun, M.D., Ph.D</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Urologic oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhu, Chen, M.S</au><au>Shao, Pengfei, M.D., Ph.D</au><au>Bao, Meiling, M.S</au><au>Li, Pu, M.S</au><au>Zhou, Hai, M.S</au><au>Cai, Hongzhou, M.S</au><au>Cao, Qiang, M.S</au><au>Tao, Liangjun, M.S</au><au>Meng, Xiaoxin, M.D., Ph.D</au><au>Ju, Xiaobing, M.D., Ph.D</au><au>Qin, Chao, M.D., Ph.D</au><au>Li, Jie, M.D., Ph.D</au><au>Yin, Changjun, M.D., Ph.D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>miR-154 inhibits prostate cancer cell proliferation by targeting CCND2</atitle><jtitle>Urologic oncology</jtitle><addtitle>Urol Oncol</addtitle><date>2014</date><risdate>2014</risdate><volume>32</volume><issue>1</issue><spage>31.e9</spage><epage>31.e16</epage><pages>31.e9-31.e16</pages><issn>1078-1439</issn><eissn>1873-2496</eissn><abstract>Abstract Background Research has shown reduced expression levels of miR-154 in prostate cancer (CaP). However, the function and molecular mechanisms of miR-154 in this cancer type remains unknown. Objective The aims of this study were to examine the functional significance of miR-154 in CaP cells and to identify the novel molecular targets regulated by miR-154. Materials and methods miR-154 expression significantly decreased in primary CaP samples compared with nonmalignant samples measured by quantitative reverse transcription polymerase chain reaction. Restoration of miR-154 lowered the potential of CaP cell lines to grow and proliferate in vitro evaluated by CCK-8 assay, colony formation assay, and flow cytometry. miR-154 down-regulated the expression of CCND2 by binding to its 3′-untranslated region by luciferase reporter assay. Conclusions miR-154 plays a prominent role in CaP proliferation by suppressing CCND2, and it may provide a new approach to the treatment of CaP.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>23428540</pmid><doi>10.1016/j.urolonc.2012.11.013</doi></addata></record> |
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| subjects | Aged CCND2 Cell Cycle Cell Enlargement Cell Line, Tumor Cell Proliferation Cyclin D2 - metabolism Gene Expression Regulation, Neoplastic Humans Male MicroRNAs - physiology Middle Aged miR-154 Prostate cancer Prostatic Neoplasms - genetics Prostatic Neoplasms - metabolism Urology |
| title | miR-154 inhibits prostate cancer cell proliferation by targeting CCND2 |
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