In a genetic screen in Drosophila designed to identify genes that enhance or restrict Notch-induced tumorigenesis, the microRNA gene Dmel\mir-8 was identified as an inhibitor of Notch-induced overgrowth and tumor metastasis. Overexpression and loss-of-function mutations of mir-8 result in developmental defects similar to those observed with impaired Notch signalling. It was determined that mir-8 directly inhibits the translation of the Notch ligand Serrate (Ser) and that overexpression of Ser rescues the growth defect produced by mir-8 overexpression.
Extending these experiments to the orthologous genes in human, it was found that MIR200C and MIR141 directly inhibit JAGGED1. In a metastatic prostate cancer cell line, overexpression of the miRNAs decreased JAG1 protein levels and impeded cell growth.
[updated May 2019 by FlyBase; FBrf0222196]
Notch signaling is an evolutionarily conserved intercellular signaling pathway that participates in critical processes throughout development, from embryogenesis to determination of adult stem cells. Activation of the Notch signaling pathway is observed in a number of cancers.
Many to one: 2 human to 1 Drosophila.
Many to one: 2 human to 1 Drosophila.
High-scoring ortholog of human JAG1 and JAG2 (1 Drosophila to 2 human). Dmel\Ser shares 33-35% identity and 46% similarity with the human genes.
Orthologous to human MIR200B, MIR200C, MIR141 and others (FBrf0242402).