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RESEARCH PRODUCT
Erratum: By promoting cell differentiation, miR-100 sensitizes basal-like breast cancer stem cells to hormonal therapy
Annalisa PetrelliRosachiara CarolloMarilisa CargneluttiFlora IovinoMaurizio CallariDaniela CiminoMatilde TodaroLaura Rosa MangiapaneAlessandro GiammonaAdriana CordovaFilippo MontemurroDaniela TavernaMaria Grazia DaidoneGiorgio StassiSilvia Giordanosubject
AdultAntineoplastic Agents HormonalTransplantation HeterologousBreast cancer basal-like differentiation miR-100Breast NeoplasmsCell Cycle ProteinsKaplan-Meier EstimateMice SCIDProtein Serine-Threonine KinasesMice Inbred NODCell Line TumorProto-Oncogene ProteinsAnimalsHumansAgedAged 80 and overReverse Transcriptase Polymerase Chain ReactionCorrectionCell DifferentiationMiddle AgedPrognosisImmunohistochemistryGene Expression Regulation NeoplasticMicroRNAsTamoxifenOncologyReceptors EstrogenMCF-7 CellsNeoplastic Stem CellsFemaledescription
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.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2019-08-13 |