microRNA-155 promotes the proliferation of prostate cancer cells by targeting annexin 7
Micro (mi)RNAs are a group of small non-coding RNA molecules that have been demonstrated to regulate the expression of genes involved in tumorigenesis. The relevance of microRNAs in the development, progression and prognosis of prostate cancer is not fully understood. miR-155 has been implicated in...
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| Veröffentlicht in: | Molecular medicine reports 2015-01, Vol.11 (1), p.533-538 |
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| creator | CAI, ZHI-KANG CHEN, QI CHEN, YAN-BO GU, MENG ZHENG, DA-CHAO ZHOU, JUAN WANG, ZHONG |
| description | Micro (mi)RNAs are a group of small non-coding RNA molecules that have been demonstrated to regulate the expression of genes involved in tumorigenesis. The relevance of microRNAs in the development, progression and prognosis of prostate cancer is not fully understood. miR-155 has been implicated in the induction of breast, lung and liver cancer, but its role in prostate cancer has not been investigated. In the present study, the biological function of miR-155 was investigated in prostate cancer for the first time, to the best of our knowledge. It was demonstrated that the expression of miR-155 was upregulated in prostate cancer tissues and cell lines as determined by quantitative reverse transcription-polymerase chain reaction. Furthermore, overexpression of miR-155 promoted cell proliferation, as indicated by MTT assay. Flow cytometric analysis demonstrated that inhibition of miR-155 induced cell cycle arrest and promoted apoptosis in prostate cancer cells. In addition, western blot analysis indicated that annexin (ANX)7 was significantly downregulated in prostate cancer tissues and cells. A luciferase reporter assay indicated that ANX7 was a target of miR-155, which suggested that miRNA-155 promoted the proliferation of prostate cancer cells by regulating ANX7 expression levels. |
| doi_str_mv | 10.3892/mmr.2014.2744 |
| format | Article |
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The relevance of microRNAs in the development, progression and prognosis of prostate cancer is not fully understood. miR-155 has been implicated in the induction of breast, lung and liver cancer, but its role in prostate cancer has not been investigated. In the present study, the biological function of miR-155 was investigated in prostate cancer for the first time, to the best of our knowledge. It was demonstrated that the expression of miR-155 was upregulated in prostate cancer tissues and cell lines as determined by quantitative reverse transcription-polymerase chain reaction. Furthermore, overexpression of miR-155 promoted cell proliferation, as indicated by MTT assay. Flow cytometric analysis demonstrated that inhibition of miR-155 induced cell cycle arrest and promoted apoptosis in prostate cancer cells. In addition, western blot analysis indicated that annexin (ANX)7 was significantly downregulated in prostate cancer tissues and cells. A luciferase reporter assay indicated that ANX7 was a target of miR-155, which suggested that miRNA-155 promoted the proliferation of prostate cancer cells by regulating ANX7 expression levels.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2014.2744</identifier><identifier>PMID: 25339368</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>3' Untranslated Regions ; Analysis ; annexin 7 ; Annexin A7 - genetics ; Apoptosis ; Apoptosis - genetics ; Breast cancer ; Cancer cells ; Cell adhesion & migration ; Cell cycle ; Cell Cycle Checkpoints - genetics ; Cell division ; Cell growth ; Cell Line, Tumor ; Cell Proliferation ; Development and progression ; Flow cytometry ; Gene Expression Regulation, Neoplastic ; Humans ; Kinases ; Liver cancer ; Lung cancer ; Male ; Medical prognosis ; MicroRNA ; MicroRNAs - genetics ; miR-155 ; miRNA ; Non-coding RNA ; Physiological aspects ; Polymerase chain reaction ; Prostate cancer ; Prostatic Neoplasms - genetics ; Proteins ; Reverse transcription ; RNA Interference ; Tumor cell lines ; Tumorigenesis</subject><ispartof>Molecular medicine reports, 2015-01, Vol.11 (1), p.533-538</ispartof><rights>Copyright © 2015, Spandidos Publications</rights><rights>COPYRIGHT 2015 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c562t-21ef57babefc35e3d14693c0d7e44d7a60c7490bd6f5b57785ff43db4ab656173</citedby><cites>FETCH-LOGICAL-c562t-21ef57babefc35e3d14693c0d7e44d7a60c7490bd6f5b57785ff43db4ab656173</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,5570,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25339368$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>CAI, ZHI-KANG</creatorcontrib><creatorcontrib>CHEN, QI</creatorcontrib><creatorcontrib>CHEN, YAN-BO</creatorcontrib><creatorcontrib>GU, MENG</creatorcontrib><creatorcontrib>ZHENG, DA-CHAO</creatorcontrib><creatorcontrib>ZHOU, JUAN</creatorcontrib><creatorcontrib>WANG, ZHONG</creatorcontrib><title>microRNA-155 promotes the proliferation of prostate cancer cells by targeting annexin 7</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Micro (mi)RNAs are a group of small non-coding RNA molecules that have been demonstrated to regulate the expression of genes involved in tumorigenesis. The relevance of microRNAs in the development, progression and prognosis of prostate cancer is not fully understood. miR-155 has been implicated in the induction of breast, lung and liver cancer, but its role in prostate cancer has not been investigated. In the present study, the biological function of miR-155 was investigated in prostate cancer for the first time, to the best of our knowledge. It was demonstrated that the expression of miR-155 was upregulated in prostate cancer tissues and cell lines as determined by quantitative reverse transcription-polymerase chain reaction. Furthermore, overexpression of miR-155 promoted cell proliferation, as indicated by MTT assay. Flow cytometric analysis demonstrated that inhibition of miR-155 induced cell cycle arrest and promoted apoptosis in prostate cancer cells. In addition, western blot analysis indicated that annexin (ANX)7 was significantly downregulated in prostate cancer tissues and cells. A luciferase reporter assay indicated that ANX7 was a target of miR-155, which suggested that miRNA-155 promoted the proliferation of prostate cancer cells by regulating ANX7 expression levels.</description><subject>3' Untranslated Regions</subject><subject>Analysis</subject><subject>annexin 7</subject><subject>Annexin A7 - genetics</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Breast cancer</subject><subject>Cancer cells</subject><subject>Cell adhesion & migration</subject><subject>Cell cycle</subject><subject>Cell Cycle Checkpoints - genetics</subject><subject>Cell division</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Development and progression</subject><subject>Flow cytometry</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Kinases</subject><subject>Liver cancer</subject><subject>Lung cancer</subject><subject>Male</subject><subject>Medical prognosis</subject><subject>MicroRNA</subject><subject>MicroRNAs - genetics</subject><subject>miR-155</subject><subject>miRNA</subject><subject>Non-coding RNA</subject><subject>Physiological aspects</subject><subject>Polymerase chain reaction</subject><subject>Prostate cancer</subject><subject>Prostatic Neoplasms - genetics</subject><subject>Proteins</subject><subject>Reverse transcription</subject><subject>RNA Interference</subject><subject>Tumor cell lines</subject><subject>Tumorigenesis</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</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>eNptkc1rFDEUwAex2Fo9epWAB0-zzXdmjkupH1AsiOIxZJKXNWUmWZMs2P--GXYtCpJAksfvvTzer-veELxhw0ivliVvKCZ8QxXnz7oLokbSM4z589OdjqM6716Wco-xFFSML7pzKhgbmRwuuh9LsDl9_bLtiRBon9OSKhRUf8L6mIOHbGpIESW_Bko1FZA10UJGFua5oOkBVZN3UEPcIRMj_A4RqVfdmTdzgden87L7_uHm2_Wn_vbu4-fr7W1vhaS1pwS8UJOZwFsmgDnC5cgsdgo4d8pIbBUf8eSkF5NQahDec-YmbiYpJFHssnt3rNua-3WAUvV9OuTYvtRkZJRLMQx_UTszgw7Rp5qNXUKxessxYQNmnDZq8x-qLQdtSimCDy3-T0J_TGgjLCWD1_scFpMfNMF6taObHb3a0audxr89NXuYFnBP9B8dDXh_BMreRBdcKk9Mq9QT0uO2G80eAb-QleE</recordid><startdate>20150101</startdate><enddate>20150101</enddate><creator>CAI, ZHI-KANG</creator><creator>CHEN, QI</creator><creator>CHEN, YAN-BO</creator><creator>GU, MENG</creator><creator>ZHENG, DA-CHAO</creator><creator>ZHOU, JUAN</creator><creator>WANG, ZHONG</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>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20150101</creationdate><title>microRNA-155 promotes the proliferation of prostate cancer cells by targeting annexin 7</title><author>CAI, ZHI-KANG ; CHEN, QI ; CHEN, YAN-BO ; GU, MENG ; ZHENG, DA-CHAO ; ZHOU, JUAN ; WANG, ZHONG</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c562t-21ef57babefc35e3d14693c0d7e44d7a60c7490bd6f5b57785ff43db4ab656173</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>3' Untranslated Regions</topic><topic>Analysis</topic><topic>annexin 7</topic><topic>Annexin A7 - genetics</topic><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Breast cancer</topic><topic>Cancer cells</topic><topic>Cell adhesion & migration</topic><topic>Cell cycle</topic><topic>Cell Cycle Checkpoints - genetics</topic><topic>Cell division</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Development and progression</topic><topic>Flow cytometry</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Kinases</topic><topic>Liver cancer</topic><topic>Lung cancer</topic><topic>Male</topic><topic>Medical prognosis</topic><topic>MicroRNA</topic><topic>MicroRNAs - genetics</topic><topic>miR-155</topic><topic>miRNA</topic><topic>Non-coding RNA</topic><topic>Physiological aspects</topic><topic>Polymerase chain reaction</topic><topic>Prostate cancer</topic><topic>Prostatic Neoplasms - genetics</topic><topic>Proteins</topic><topic>Reverse transcription</topic><topic>RNA Interference</topic><topic>Tumor cell lines</topic><topic>Tumorigenesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>CAI, ZHI-KANG</creatorcontrib><creatorcontrib>CHEN, QI</creatorcontrib><creatorcontrib>CHEN, YAN-BO</creatorcontrib><creatorcontrib>GU, MENG</creatorcontrib><creatorcontrib>ZHENG, DA-CHAO</creatorcontrib><creatorcontrib>ZHOU, JUAN</creatorcontrib><creatorcontrib>WANG, ZHONG</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>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science 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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection (ProQuest)</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science 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><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>CAI, ZHI-KANG</au><au>CHEN, QI</au><au>CHEN, YAN-BO</au><au>GU, MENG</au><au>ZHENG, DA-CHAO</au><au>ZHOU, JUAN</au><au>WANG, ZHONG</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>microRNA-155 promotes the proliferation of prostate cancer cells by targeting annexin 7</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2015-01-01</date><risdate>2015</risdate><volume>11</volume><issue>1</issue><spage>533</spage><epage>538</epage><pages>533-538</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Micro (mi)RNAs are a group of small non-coding RNA molecules that have been demonstrated to regulate the expression of genes involved in tumorigenesis. The relevance of microRNAs in the development, progression and prognosis of prostate cancer is not fully understood. miR-155 has been implicated in the induction of breast, lung and liver cancer, but its role in prostate cancer has not been investigated. In the present study, the biological function of miR-155 was investigated in prostate cancer for the first time, to the best of our knowledge. It was demonstrated that the expression of miR-155 was upregulated in prostate cancer tissues and cell lines as determined by quantitative reverse transcription-polymerase chain reaction. Furthermore, overexpression of miR-155 promoted cell proliferation, as indicated by MTT assay. Flow cytometric analysis demonstrated that inhibition of miR-155 induced cell cycle arrest and promoted apoptosis in prostate cancer cells. In addition, western blot analysis indicated that annexin (ANX)7 was significantly downregulated in prostate cancer tissues and cells. A luciferase reporter assay indicated that ANX7 was a target of miR-155, which suggested that miRNA-155 promoted the proliferation of prostate cancer cells by regulating ANX7 expression levels.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>25339368</pmid><doi>10.3892/mmr.2014.2744</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | 3' Untranslated Regions Analysis annexin 7 Annexin A7 - genetics Apoptosis Apoptosis - genetics Breast cancer Cancer cells Cell adhesion & migration Cell cycle Cell Cycle Checkpoints - genetics Cell division Cell growth Cell Line, Tumor Cell Proliferation Development and progression Flow cytometry Gene Expression Regulation, Neoplastic Humans Kinases Liver cancer Lung cancer Male Medical prognosis MicroRNA MicroRNAs - genetics miR-155 miRNA Non-coding RNA Physiological aspects Polymerase chain reaction Prostate cancer Prostatic Neoplasms - genetics Proteins Reverse transcription RNA Interference Tumor cell lines Tumorigenesis |
| title | microRNA-155 promotes the proliferation of prostate cancer cells by targeting annexin 7 |
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