000			nab a22 7a 4500
999			_c16737 _d16737
003			PC16737
005			20220302115441.0
008			220302b xxu||||| |||| 00| 0 eng d
040			_cH12O
041			_aeng
100			_92806 _aMartínez Fernández, Mónica _eInstituto de Investigación i+12
100			_92807 _aDueñas, Marta _eInstituto de Investigación i+12
100			_92996 _aSegovia, Cristina _eInstituto de Investigación imas12
100			_92683 _aGarcía Escudero, Ramón _eInstituto de Investigación i+12
100			_92997 _aRubio, Carolina _eInstituto de Investigación imas12
100			_92998 _aLópez Calderón, Fernando F _eInstituto de Investigación imas12
100			_9485 _aVillacampa Aubá, Felipe _eUrología
100			_91980 _aDuarte Ojeda, José Manuel _eUrología
100			_92810 _aGómez Rodríguez, María José _eUrología
100			_9882 _aCastellano, Daniel _eOncología Médica
100			_91219 _aRodríguez Peralto, José Luis _eAnatomía Patológica
100			_91795 _aRosa Kehrman, Federico de la _eUrología
100			_92814 _aParamio, Jesús M. _eInstituto de Investigación i+12
245			_aA Polycomb-mir200 loop regulates clinical outcome in bladder cancer. _h[artículo]
260			_bOncotarget, _c2015
500			_aFormato Vancouver: Martínez Fernández M, Dueñas M, Feber A, Segovia C, García Escudero R, Rubio C et al. A Polycomb-mir200 loop regulates clinical outcome in bladder cancer. Oncotarget.2015 Dec 8;6(39):42258-75.
501			_aPMID: 26517683 PMCID: PMC4747223.
504			_aContiene 66 referencias
520			_aBladder cancer (BC) is a highly prevalent disease, ranking fifth in the most common cancers worldwide. Various miRNAs have recently emerged as potential prognostic biomarkers in cancer. The miR-200 family, which repressed the epithelial-to-mesenchymal transition (EMT), is repressed in multiple advanced cancers. However, its expression and function in BC is still poorly understood. Here we show that miR-200 family displays increased expression, probably due to the activation of specific oncogenic signaling pathways, and reduced promoter methylation, in BC compared to normal bladder samples. Furthermore, we show that the expression of these miRNAs is decreased in high grade and stage tumors, and the down-regulation is associated with patient's poor clinical outcome. Our data indicate that the miR-200 family plays distinct roles in Non-Muscle (NMIBC) and Muscle-Invasive BC (MIBC). In MIBC, miR-200 expression post transcriptionally regulates EMT-promoting transcription factors ZEB1 and ZEB2, whereas suppresses BMI1 expression in NMIBC. Interestingly, we show that increased EZH2 and/or BMI1 expression repress the expression of miR-200 family members. Collectively, these findings support a model of BC progression through a coordinated action between the Polycomb Repression Complex (PRC) members repressing the miR-200 expression, which ultimately favors invasive BC development. Since pharmacological inhibition of EZH2 in BC cell lines lead to increased miR-200 expression, our findings may support new therapeutic strategies for BC clinical management.
710			_9625 _aInstituto de Investigación imas12
710			_9220 _aServicio de Urología
710			_9303 _aServicio de Oncología Médica
710			_9330 _aServicio de Anatomía Patológica
856			_uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4747223/ _yAcceso libre
942			_2ddc _cART _n0