miR-21 may acts as an oncomir by targeting RECK, a matrix metalloproteinase regulator, in prostate cancer

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dc.contributor Sistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.author REIS, Sabrina Thalita FMUSP-HC
PONTES-JUNIOR, Jose FMUSP-HC
ANTUNES, Alberto Azoubel FMUSP-HC
DALL'OGLIO, Marcos Francisco FMUSP-HC
DIP, Nelson FMUSP-HC
PASSEROTTI, Carlo Camargo FMUSP-HC
ROSSINI, Guilherme Ayres
MORAIS, Denis Reis FMUSP-HC
NESRALLAH, Adriano Joao FMUSP-HC
PIANTINO, Camila FMUSP-HC
SROUGI, Miguel FMUSP-HC
LEITE, Katia R. FMUSP-HC
dc.date.issued 2012
dc.identifier.citation BMC UROLOGY, v.12, article ID 14, 7p, 2012
dc.identifier.issn 1471-2490
dc.identifier.uri http://observatorio.fm.usp.br/handle/OPI/329
dc.description.abstract Background: Prognosis of prostate cancer (PCa) is based mainly in histological aspects together with PSA serum levels that not always reflect the real aggressive potential of the neoplasia. The micro RNA (miRNA) mir-21 has been shown to regulate invasiveness in cancer through translational repression of the Metaloproteinase (MMP) inhibitor RECK. Our aim is to investigate the levels of expression of RECK and miR-21 in PCa comparing with classical prognostic factors and disease outcome and also test if RECK is a target of miR-21 in in vitro study using PCa cell line. Materials and methods: To determine if RECK is a target of miR-21 in prostate cancer we performed an in vitro assay with PCa cell line DU-145 transfected with pre-miR-21 and anti-miR-21. To determine miR-21 and RECK expression levels in PCa samples we performed quantitative real-time polymerase chain reaction (qRT-PCR). Results: The in vitro assays showed a decrease in expression levels of RECK after transfection with pre-miR-21, and an increase of MMP9 that is regulated by RECK compared to PCa cells treated with anti-miR-21. We defined three profiles to compare the prognostic factors. The first was characterized by miR-21 and RECK underexpression (N = 25) the second was characterized by miR-21 overexpression and RECK underexpression (N = 12), and the third was characterized by miR-21 underexpression and RECK overexpression (N = 16). From men who presented the second profile (miR-21 overexpression and RECK underexpression) 91.7% were staged pT3. For the other two groups 48.0%, and 46.7% of patients were staged pT3 (p = 0.025). Conclusions: Our results demonstrate RECK as a target of miR-21. We believe that miR-21 may be important in PCa progression through its regulation of RECK, a known regulator of tumor cell invasion.
dc.description.sponsorship · FAPESP (Fundacao de Amparo a Pesquisa do Estado de Sao Paulo) [2009/50368-9]
dc.language.iso eng
dc.publisher BIOMED CENTRAL LTD
dc.relation.ispartof BMC Urology
dc.rights openAccess
dc.subject Prostate cancer; Prognosis; RECK; Micro RNA; Metaloproteinases
dc.subject.other tumor-suppressor gene; microrna-21 targets; lung-cancer; expression; invasion; metastasis; oncogenes; puzzle; cells; piece
dc.title miR-21 may acts as an oncomir by targeting RECK, a matrix metalloproteinase regulator, in prostate cancer
dc.type article
dc.rights.holder Copyright BIOMED CENTRAL LTD
dc.description.group LIM/55
dc.identifier.doi 10.1186/1471-2490-12-14
dc.identifier.pmid 22642976
dc.type.category original article
dc.type.version publishedVersion
hcfmusp.author REIS, Sabrina Thalita:HC:LIM/55
hcfmusp.author PONTES-JUNIOR, Jose:HC:ICHC
hcfmusp.author ANTUNES, Alberto Azoubel:HC:LIM/55
hcfmusp.author DALL'OGLIO, Marcos Francisco:FM:MCG
hcfmusp.author DIP, Nelson:FM:
hcfmusp.author PASSEROTTI, Carlo Camargo:HC:ICHC
hcfmusp.author MORAIS, Denis Reis:FM:
hcfmusp.author NESRALLAH, Adriano Joao:HC:ICESP
hcfmusp.author PIANTINO, Camila:FM:
hcfmusp.author SROUGI, Miguel:FM:MCG
hcfmusp.author LEITE, Katia R.:HC:LIM/55
hcfmusp.author.external · ROSSINI, Guilherme Ayres:Nove de Julho Univ, Dept Urol, Sao Paulo, Brazil
hcfmusp.origem.id 2-s2.0-84861474291
hcfmusp.origem.id WOS:000313240000001
hcfmusp.publisher.city LONDON
hcfmusp.publisher.country ENGLAND
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dc.description.index MEDLINE
hcfmusp.citation.scopus 78
hcfmusp.citation.wos 67
hcfmusp.affiliation.country Brasil


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