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Oncogene. 2014 Aug 28;33(35):4377-84. doi: 10.1038/onc.2013.407. Epub 2013 Oct 7.

Cell competition may function either as tumour-suppressing or as tumour-stimulating factor in Drosophila.

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1
Centro de BiologĂ­a Molecular, CSIC-Universidad Autonoma de Madrid, Madrid, Spain.

Abstract

Drosophila endocytosis-defective cells develop tumour overgrowths in the imaginal discs. We have analysed the tumorigenic potential of cells mutant for Rab5, a gene involved in endocytosis. We found that while a compartment entirely made by Rab5 mutant cells can grow indefinitely, clones of Rab5 cells surrounded by normal cells are eliminated by cell competition. However, when a group of about 400 cells are simultaneously made mutant for Rab5, they form an overgrowing tumour: mutant cells in the periphery are eliminated, but those inside survive and continue proliferating because they are beyond the range of cell competition. These results identify group protection as a mechanism to evade the tumour-suppressing function of cell competition in Drosophila. Furthermore, we find that the growth of the tumour depends to a large extent on the presence of apoptosis inside the tumour: cells doubly mutant for Rab5 and the proapoptotic gene dronc do not form overgrowing tumours. These results suggest that the apoptosis caused by cell competition acts as a tumour-stimulating factor, bringing about high levels of Jun N-terminal kinase and subsequently Wg/Dpp signalling and high proliferation levels in the growing tumour. We conclude that under these circumstances cell competition facilitates the progression of the tumour, thus reversing its normal antitumour role.

PMID:
24096487
DOI:
10.1038/onc.2013.407
[Indexed for MEDLINE]
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