MiR-221 promotes stemness of breast cancer cells by targeting DNMT3b

Matilde Todaro, Miriam Gaggianesi, Manel Esteller, Renato Thomas, Giulia Romano, Cristina Quintavalle, Angel Diaz-Lagares, Margherita Iaboni, Miriam Gaggianesi, Giulia Romano, Giuseppina Roscigno, Elvira Donnarumma, Valentina Russo, Ilaria Puoti, Valentina Russo, Gerolama Condorelli, Matilde Todaro, Danilo Fiore, Carlo M. Croce, Giuseppina Cortino

Risultato della ricerca: Articlepeer review

62 Citazioni (Scopus)

Abstract

Cancer stem cells (CSCs) are a small part of the heterogeneous tumor cell population possessing self-renewal and multilineage differentiation potential as well as a great ability to sustain tumorigenesis. The molecular pathways underlying CSC phenotype are not yet well characterized. MicroRNAs (miRs) are small noncoding RNAs that play a powerful role in biological processes. Early studies have linked miRs to the control of self-renewal and differentiation in normal and cancer stem cells. We aimed to study the functional role of miRs in human breast cancer stem cells (BCSCs), also named mammospheres. We found that miR-221 was upregulated in BCSCs compared to their differentiated counterpart. Similarly, mammospheres from T47D cells had an increased level of miR-221 compared to differentiated cells. Transfection of miR-221 in T47D cells increased the number of mammospheres and the expression of stem cell markers. Among miR-221's targets, we identified DNMT3b. Furthermore, in BCSCs we found that DNMT3b repressed the expression of various stemness genes, such as Nanog and Oct 3/4, acting on the methylation of their promoters, partially reverting the effect of miR-221 on stemness. We hypothesize that miR-221 contributes to breast cancer tumorigenicity by regulating stemness, at least in part through the control of DNMT3b expression.
Lingua originaleEnglish
pagine (da-a)580-592
Numero di pagine13
RivistaOncotarget
Volume7
Stato di pubblicazionePublished - 2016

All Science Journal Classification (ASJC) codes

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