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Ovarian Tumors in Rbp9 Mutants of Drosophila Induce an Immune Response  

Kim, Jihyun (Department of Molecular Biology, School of Natural Sciences, Sejong University)
Kim, Chun (Cutaneous Biology Research Center, Massachusetts General Hospital, Harvard Medical School)
Kim-Ha, Jeongsil (Department of Molecular Biology, School of Natural Sciences, Sejong University)
Abstract
The Drosophila protein, Rbp9, is homologous to human Hu, which is reported to be involved in small cell lung cancer. Rbp9 functions in cystocyte differentiation, and mutations in Rbp9 cause ovarian tumors. Here we show that the antimicrobial peptide, Attacin, is upregulated in Rbp9 mutants, especially in ovaries where tumors form. Upregulation seems to result from activation of the NF-${\kappa}B$ pathway since we detected nuclear localization of Relish in Rbp9 mutant ovaries but not in wild type ovaries. Inactivation of NF-${\kappa}B$ in the Rbp9 mutant allows prolonged survival of malformed egg chambers. We conclude that Drosophila initiates an anti-tumor defense response via activation of NF-${\kappa}B$.
Keywords
Antimicrobial Peptides; NF-${\kappa}B$; Ovarian Tumor; Rbp9;
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