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Poster display session

5288 - Stimulation of RAC1/PAK1 signalling upregulates DNA damage repair genes via the BCL6/STAT5-switch


11 Sep 2017


Poster display session


Cancer Biology


Patrícia Barros


Annals of Oncology (2017) 28 (suppl_5): v1-v21. 10.1093/annonc/mdx361


P. Barros1, A.J. Amaral1, L.B. Abrantes1, T. Oliveira1, H. Louro2, M.J. Silva2, P. Jordan2, M. Gama-Carvalho1, P. Matos1

Author affiliations

  • 1 Bioisi, University of Lisboa, Faculty of Sciences, BioISI – Biosystems & Integrative Sciences Institute, 1749-016 - Lisboa/PT
  • 2 Departamento De Genética Humana, Instituto Nacional de Saúde, Doutor Ricardo Jorge, 1649-016 - Lisboa/PT


Abstract 5288


Colorectal cancer is one of the most prevalent types of cancer worldwide. The GTPase RAC1 and its effector PAK1 have been found overexpressed or hyperactivated in this type of cancers, particularly those with more aggressive and invasive features, which is frequently correlated with resistance to chemotherapeutics and unfavourable clinical prognosis. Previously, we described a new signalling pathway in which activation of RAC1/PAK1 signalling promotes a transcriptional switch between the BCL6 repressor and the STAT5 transcriptional activator at a restricted subset of gene promoters.


Here we used a novel combinatory ChIP-Seq approach for the genome-wide identification of the BCL6/STAT5-switch target genes.


Ontological enrichment analysis among the identified target genes revealed an overrepresentation of genes involved in DNA damage repair. Using the comet assay as readout for the extent of DNA damage, we show that the activation of RAC1/PAK1 signalling significantly accelerates DNA damage repair through the upregulation of pivotal genes.


This work highlights an additional role for the RAC1/PAK1 signalling axis that may contribute to the chemoresistant phenotype of aggressive colorectal tumours.

Clinical trial identification

Legal entity responsible for the study

Paulo Matos


Fundação para a Ciência e Tecnologia.


All authors have declared no conflicts of interest.

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