Please use this identifier to cite or link to this item: http://hdl.handle.net/2445/111613
Title: MiR-221 promotes stemness of breast cancer cells by targeting DNMT3b
Author: Roscigno, Giuseppina
Quintavalle, Cristina
Donnarumma, Elvira
Puoti, Ilaria
Diaz-Lagares, Angel
Iaboni, Margherita
Fiore, Danilo
Russo, Valentino
Todaro, Matilde
Romano, Guilia
Thomas, Renato
Cortino, Giuseppina
Gaggianesi, Miriam
Esteller, Manel
Croce, Carlo M.
Condorelli, Gerolama
Keywords: Cèl·lules mare
ADN
Micro RNAs
Càncer de mama
Stem cells
DNA
MicroRNAs
Breast cancer
Issue Date: 5-Jan-2016
Publisher: Impact Journals
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.
Note: Reproducció del document publicat a: https://doi.org/10.18632/oncotarget.5979
It is part of: Oncotarget, 2016, vol. 7, num. 1, p. 580-592
Related resource: https://doi.org/10.18632/oncotarget.5979
URI: http://hdl.handle.net/2445/111613
ISSN: 1949-2553
Appears in Collections:Articles publicats en revistes (Ciències Fisiològiques)
Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL))

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