Step by Step, understanding the background of cancer: Analysis of the protumoral role of the JNK pathway in Drosophila melanogaster
Autor: Carme Pifarré Esquerda
Centre: CLAVER
Premi: 1r Premi
Document:
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In this work, we use Drosophila melanogaster epithelial cells to address the role of CIN in tumor development. We show that depletion of spindle assembly checkpoint genes (e.g. bub3) in Drosophila leads to programmed cell death and apoptotic response, which depends on the activations of the c-Jun N-terminal kinase (JNK) signaling pathway. When we prevent cells from undergoing apoptosis with the p35 protein, CIN leads to a neoplastic overgrowth and drives tumorigenesis. The JNK transcriptional program is activated in delaminating cells and drives tissue overgrowth and invasiveness. We also showed that the blockage of the JNK pathways partially rescues CIN cells from forming a tumor. Altogether, our findings support the proposal that CIN promotes a rapid and invasive behavior in epithelial cells and reinforce the pro-tumorigenic role of the JNK pathway.