Temperature Controlled Tumorigenesis in Drosophila melanogaster

Abstract

Cancer is an age-associated disease, with metastasis being the primary cause of mortality. Innate immune cells, such as macrophages, serve as the first line of defense against tumorigenesis. However, macrophages have also been found to promote metastasis. Despite this knowledge, the mechanisms by which macrophages switch from defending against tumorigenesis to facilitating metastasis remain poorly understood. To investigate this, we use Drosophila melanogaster, which possesses a conserved innate immune system and oncogenic pathways. 

In our lab, we found that Drosophila strains with oncogenes in the Df(IRER) background, where the irradiation-responsive enhancer region was deleted, showed dramatic metastatic phenotypes. Macrophages in Df(IRER) also exhibited an accelerated aging phenotype. To better understand the exact moment when macrophages begin to facilitate cancer metastasis, we developed a temperature-sensitive system to control tumorigenesis, allowing us to monitor macrophage interactions at different stages of tumor development. Using this system, we identified configurations that can manipulate the timing of tumorigenesis in wild-type flies. 

In future experiments, we will investigate whether this temperature-controlled system also leads to metastasis in Df(IRER) background flies and monitor the behavior and role of macrophages at different stages of tumor progression. 

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