Upregulation of the interferon-inducible antiviral gene RSAD2 in neuroendocrine prostate cancer via PVT1 exon 9 dependent and independent pathways.

PVT1 exon 9 overexpression is a newly uncovered aberration in prostate cancer (PCa). We have previously demonstrated the exon 9 region of PVT1 is overexpressed in some patient PCa tissues and causes development of neuroendocrine prostate cancer (NEPC) in vitro and in vivo. In this study, we focused on elucidating downstream mechanisms induced by PVT1 exon 9 overexpression with the goal of further understanding its role in NEPC development.

ßFTZ-F1 and Matrix metalloproteinase 2 are required for fat-body remodeling in Drosophila.

During metamorphosis, holometabolous insects eliminate obsolete larval tissues via programmed cell death. In contrast, tissues required for further development are retained and often remodeled to meet the needs of the adult fly. The larval fat body is involved in fueling metamorphosis, and thus it escapes cell death and is instead remodeled during prepupal development.