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Poster Display session 3

4357 - Identification of a stemness-related gene panel associated with BET inhibition in triple negative breast cancer


30 Sep 2019


Poster Display session 3


Translational Research

Tumour Site

Breast Cancer


Eva Galan-Moya


Annals of Oncology (2019) 30 (suppl_5): v760-v796. 10.1093/annonc/mdz268


E.M. Galan-Moya1, M. Nuncia-Cantarero1, L. Serrano-Oviedo1, S. Morcillo-García1, C. Nieto-Jiménez2, M. Burgos2, B. Győrffy3, A. Ocaña4

Author affiliations

  • 1 Medical Sciences & Regional Center For Biomedical Research, University of Castilla-La Mancha, 02008 - Albacete/ES
  • 2 Oncología Traslacional, Complejo Hospitalario Universitario de Albacete, 02006 - Albacete/ES
  • 3 Institute Of Enzymology, MTA TTK Lendület Cancer Biomarker Research Group, Budapest/HU
  • 4 Drugs Development, Hospital Clínico San Carlos, 28040 - Madrid/ES


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Abstract 4357


Triple negative breast cancers (TNBC) are enriched with cells bearing stem-like features (CSC), which underlie cancer progression, thus targeting stemness could be an interesting treatment approach. In turn, the epigenetic machinery is crucial for the maintenance of the stemness phenotype. The BET family of epigenetic readers are emerging as novel targets for cancer therapy and have shown preclinical effect in breast cancer. In this work we evaluate the effect of the BET inhibitor (BETi) JQ1 on stemness in TNBC.


Transcriptomic, functional annotation and qPCR studies were performed on JQ1-exposed TNBC cells. Results were confirmed on spheroids and spheroid-derived tumours. Limiting dilution assays, matrigel invasion experiments, immunofluorescence staining, and flow cytometry studies were also performed to evaluate the effect of JQ1 on CSC features. For the outcome analysis, the online tool Kaplan-Meier Plotter and an integrated response database were used.


JQ1 can modify the expression of stemness-related genes incultured TNBC cells. Among these changes, the CD44/CD24 and ALDH1A1 expression, both classical stemness markers, were diminished by JQ1. Using a validated spheroid model, to mimic the intrinsic characteristics of CSCs, we show that JQ1 decreased surface expression of CD44, inhibited self-renewal and invasion, and induced cells arrest in G0/G1, therefore altering the stemness phenotype in TNBC. Four of the identified stemness genes, GJA1, CD24, EPCAM, and SOX9, were found to be associated with worse patient outcome in TNBC. Furthermore, ABCG2 and RUNX2 predicted low response to chemotherapy in TNBC patients.


In this work we show how BETi modify the stemness landscape in TNBC. Thus, we propose a novel role for JQ1 as a stemness-targeting drug. Loss of the stem cell phenotype via JQ1 treatment could lead to less aggressive and more chemo-sensitive tumours, which would reflect in better patient prognosis.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The authors.


Has not received any funding.


All authors have declared no conflicts of interest.

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