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<title lang=en>Androgen-regulated microRNA-135a decreases prostate cancer cell migration and invasion through downregulating ROCK1 and ROCK2</title>
<creator>Kroiss, A.</creator>
<creator>Vincent, Serge</creator>
<creator>Decaussin-Petrucci, M.</creator>
<creator>Meugnier, E.</creator>
<creator>Viallet, J.</creator>
<creator>Ruffion, A.</creator>
<creator>Chalmel, F.</creator>
<creator>Samarut, J.</creator>
<creator>Allioli, N.</creator>
<contributor>Institut de Génomique Fonctionnelle de Lyon (IGFL) ; École normale supérieure - Lyon (ENS Lyon) - Institut National de la Recherche Agronomique (INRA) - Université Claude Bernard Lyon 1 (UCBL) - Centre National de la Recherche Scientifique (CNRS)</contributor>
<contributor>Hospices Civils de Lyon / Centre hospitalier Lyon Sud (HCL) ; Hospices Civils de Lyon</contributor>
<contributor>Faculté de Médecine Lyon-Sud ; FACULTE DE LYON</contributor>
<contributor>Laboratoire de recherche en cardiovasculaire, métabolisme, diabétologie et nutrition (CarMeN) ; Institut National de la Recherche Agronomique (INRA) - Université Claude Bernard Lyon 1 (UCBL) - Institut National des Sciences Appliquées de Lyon (INSA Lyon) - Hospices Civils de Lyon - Institut National de la Santé et de la Recherche Médicale (INSERM)</contributor>
<contributor>Epidémiologie pronostique des cancers et affections graves ; Université Joseph Fourier - Grenoble 1 (UJF) - Institut National de la Santé et de la Recherche Médicale (INSERM)</contributor>
<contributor>Institut de recherche, santé, environnement et travail [Rennes] (Irset) ; Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor>
<contributor>Unité Médicale d'Oncologie Moléculaire et Transfert (UMOMT) ; Hospices Civils de Lyon</contributor>
<contributor>ISPB</contributor>
<contributor>Work was supported by grants from Institut Mérieux and the Ligue Contre le Cancer</contributor>
<description>International audience</description>
<source>ISSN: 0950-9232</source>
<source>EISSN: 1476-5594</source>
<source>Oncogene</source>
<publisher>Nature Publishing Group</publisher>
<identifier>hal-01063902</identifier>
<identifier>https://hal.archives-ouvertes.fr/hal-01063902</identifier>
<identifier>https://hal.archives-ouvertes.fr/hal-01063902/file/Androgen-regulated%20microRNA-135a.pdf</identifier>
<source>https://hal.archives-ouvertes.fr/hal-01063902</source>
<source>Oncogene, Nature Publishing Group, 2014, 34 (22), pp.2846-2855. 〈10.1038/onc.2014.222〉</source>
<identifier>DOI : 10.1038/onc.2014.222</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1038/onc.2014.222</relation>
<identifier>PUBMED : 25065599</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/25065599</relation>
<language>en</language>
<subject>[SDV] Life Sciences [q-bio]</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>Androgen signaling, via the androgen receptor (AR), is crucial in mediating prostate cancer (PCa) initiation and progression. Identifying new downstream effectors of the androgens/AR pathway will allow a better understanding of these mechanisms and could reveal novel biomarkers and/or therapeutic agents to improve the rate of patient survival. We compared the microRNA expression profiles in androgen-sensitive LNCaP cells stimulated or not with 1 nM R1881 by performing a high-throughput reverse transcriptase-quantitative PCR and found that miR-135a was upregulated. After androgen stimulation, we showed that AR directly activates the transcription of miR-135a2 gene by binding to an androgen response element in the promoter region. Our findings identify miR-135a as a novel effector in androgens/AR signaling. Using xenograft experiments in chick embryos and adult male mice, we showed that miR-135a overexpression decreases in vivo invasion abilities of prostate PC-3 cells. Through in vitro wound-healing migration and invasion assays, we demonstrated that this effect is mediated through downregulating ROCK1 and ROCK2 expression, two genes that we characterized as miR-135a direct target genes. In human surgical samples from prostatectomy, we observed that miR-135a expression was lower in tumoral compared with paired adjacent normal tissues, mainly in tumors classified with a high Gleason score (⩾8). Moreover, miR-135a expression is lower in invasive tumors, showing extraprostatic extension, as compared with intraprostatic localized tumors. In tumor relative to normal glands, we also showed a more frequently higher ROCK1 protein expression determined using a semi-quantitative immunohistochemistry analysis. Therefore, in tumor cells, the lower miR-135a expression could lead to a higher ROCK1 protein expression, which could explain their invasion abilities. The highlighted relationship between miR-135a expression level and the degree of disease aggressiveness suggests that miR-135a may be considered as a prognostic marker in human PCa.Oncogene advance online publication, 28 July 2014; doi:10.1038/onc.2014.222.</description>
<date>2014</date>
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