This model of prostate cancer is based on the observation that the Drosophila adult male accessory gland acts as a functional homolog of the mammalian prostate. It was hypothesized that normal cell growth and migration of secondary cells in the accessory gland may be regulated by Drosophila orthologs of known regulators of human prostate cancer progression. The fly gene prd is orthologous to multiple human PAX genes, including PAX2, which may promote cell growth and migration of prostate cancer cells. (FBrf0226167)
Dmel\prd is the eponymous member of the paired-type homeodomain family of transcription factors, and is orthologous to multiple human genes. It is a high-scoring ortholog of PAX3 and PAX7, both of which have been introduced into flies (see Hsap\PAX3 and Hsap\PAX7); it is a low-scoring ortholog of PAX2, which has not been introduced into flies.
Amorphic mutations of Dmel\prd result in embryonic lethality. For assessment of function in the accessory gland, RNAi-mediated knockdown of prd was controlled by using a temperature-sensitive driver and targeting newly eclosed, newly mated males. Knockdown of prd results in a significant decrease in the number of secondary cells compared to controls; the phenotype is variable with incomplete penetrance. Genetic interactions of Dmel\prd have been characterized; see the gene report for prd.
[updated Dec. 2016 by FlyBase; FBrf0222196]
Prostate cancer is the most common cancer in American men and is usually very slowly progressive; it is diagnosed in an estimated 80% of men who reach age 80 (http://www.webmd.com/prostate-cancer; 2016.12.20).
Many to many.
Many to many.
High-scoring ortholog of human PAX3 and PAX7; low-scoring ortholog of PAX2 and multiple others (many Drosophila to many human). Dmel\prd shares 41-45% identity and 50-56% similarity with human PAX3 and PAX7; it shares 32% identity and 43% similarity with PAX2.