Journal
EMBO REPORTS
Volume 14, Issue 2, Pages 172-177Publisher
WILEY
DOI: 10.1038/embor.2012.217
Keywords
Drosophila; invasion; caspase; apoptosis; JNK
Categories
Funding
- National Institutes of Health [NCI R01 CA109730, 5R01EY011495]
- [5T32CA078207]
- [5T32GM007280]
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Tumours evolve several mechanisms to evade apoptosis, yet many resected carcinomas show significantly elevated caspase activity. Moreover, caspase activity is positively correlated with tumour aggression and adverse patient outcome. These observations indicate that caspases might have a functional role in promoting tumour invasion and metastasis. Using a Drosophila model of invasion, we show that precise effector caspase activity drives cell invasion without initiating apoptosis. Affected cells express the matrix metalloproteinase Mmp1 and invade by activating Jnk. Our results link Jnk and effector caspase signalling during the invasive process and suggest that tumours under apoptotic stresses from treatment, immune surveillance or intrinsic signals might be induced further along the metastatic cascade.
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