Metastatic tumours are characterised by a high degree of chromosomal instability—that is to say a constant change in the number and structure of chromosomes they hold. In spite of this observation, it is unknown whether chromosomal instability contributes to the metastatic process. A study at the Institute for Research in Biomedicine (IRB Barcelona) using Drosophila melanogaster has demonstrated that chromosomal instability itself can induce invasive behaviour in epithelial cells and has identified the underlying molecular mechanisms involved.
To perform this study, the team directed by ICREA researcher Marco Milán generated a fruit fly model with chromosomal instability. “The cells started to actively invade adjacent tissues,” explains Marco Milán, group leader of the Growth Control and Development lab at IRB Barcelona and head of the study.
The aim was to study whether chromosomal instability itself has the capacity to stimulate invasive behaviour in epithelial cells. The results, published in Developmental Cell, indicate that this is the case, and describe a series of molecular and cell mechanisms that favour cell migration and invasion of other tissues. In particular, the researchers have demonstrated that invasive cells use the actin cytoskeleton and activate the ERK and JNK signalling pathways to trigger a pro-invasive transcriptional programme executed by the oncogene Fos and repressed by the tumour suppressor Capicua.
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