Rounding up the Usual Suspects: Assessing Yorkie, AP-1, and Stat Coactivation in Tumorigenesis

摘要: Can hyperactivation of a few key signaling effectors be the underlying reason for majority epithelial cancers despite different driver mutations? Here, to address this question, we use Drosophila model, which allows analysis gene expression from tumors with known initiating mutations. Furthermore, its simplified pathways have numerous well characterized targets can as pathway readouts. In tumor models, changes in activities three pathways, Jun N-terminal Kinase (JNK), Janus Kinase/Signal Transducer and Activator Transcription (JAK/STAT), Hippo, mediated by AP-1 factors, Stat92E, Yorkie, are reported frequently. We hypothesized may indicate that these commonly deregulated tumors. To assess this, mined available transcriptomic data evaluated activity levels eight various models. Indeed, at least two out our suspects contribute development all cancer models assessed, mutations or tissues origin. Surprisingly, found Notch is also globally activated examined. propose four JNK, JAK/STAT, Notch, paid special attention assayed systematically existing newly developed