Oncotarget

Research Papers:

This article has been corrected. Correction in: Oncotarget. 2019; 10:4920-4920.

By promoting cell differentiation, miR-100 sensitizes basal-like breast cancer stem cells to hormonal therapy

Annalisa Petrelli, Rosachiara Carollo, Marilisa Cargnelutti, Flora Iovino, Maurizio Callari, Daniela Cimino, Matilde Todaro, Laura Rosa Mangiapane, Alessandro Giammona, Adriana Cordova, Filippo Montemurro, Daniela Taverna, Maria Grazia Daidone, Giorgio Stassi and Silvia Giordano _

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Oncotarget. 2015; 6:2315-2330. https://doi.org/10.18632/oncotarget.2962

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Abstract

Annalisa Petrelli1,*, Rosachiara Carollo2,*, Marilisa Cargnelutti1, Flora Iovino2, Maurizio Callari3, Daniela Cimino4, Matilde Todaro2, Laura Rosa Mangiapane2, Alessandro Giammona2, Adriana Cordova2, Filippo Montemurro1, Daniela Taverna4, Maria Grazia Daidone3, Giorgio Stassi2,* and Silvia Giordano1,*

1 University of Torino School of Medicine, Candiolo Cancer Institute-FPO, IRCCS, Str. Provinciale, Candiolo, Torino, Italy

2 Department of Surgical and Oncological Sciences, Cellular and Molecular Pathophysiology Laboratory, University of Palermo, Palermo, Italy

3 Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy

4 Molecular Biotechnology Center (MBC), Department of Oncological Sciences, Center for Molecular Systems Biology, Via Nizza, University of Torino, Torino, Italy

* These authors contributed equally to this work

Correspondence:

Silvia Giordano, email:

Giorgio Stassi, email:

Annalisa Petrelli, email:

Keywords: Breast cancer, basal-like, differentiation, miR-100

Received: September 30, 2014 Accepted: December 10, 2014 Published: December 11, 2014

Abstract

Basal-like breast cancer is an aggressive tumor subtype with a poor response to conventional therapies. Tumor formation and relapse are sustained by a cell subset of Breast Cancer Stem Cells (BrCSCs). Here we show that miR-100 inhibits maintenance and expansion of BrCSCs in basal-like cancer through Polo-like kinase1 (Plk1) down-regulation. Moreover, miR-100 favors BrCSC differentiation, converting a basal like phenotype into luminal. It induces the expression of a functional estrogen receptor (ER) and renders basal-like BrCSCs responsive to hormonal therapy. The key role played by miR-100 in breast cancer free-survival is confirmed by the analysis of a cohort of patients’ tumors, which shows that low expression of miR-100 is a negative prognostic factor and is associated with gene signatures of high grade undifferentiated tumors. Our findings indicate a new possible therapeutic strategy, which could make aggressive breast cancers responsive to standard treatments.


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