Rounding up the usual suspects: assessing Yorkie, AP-1, and stat coactivation in tumorigenesis

Hamaratoglu, Fisun ORCID: https://orcid.org/0000-0002-1461-9248 and Atkins, Mardelle 2020. Rounding up the usual suspects: assessing Yorkie, AP-1, and stat coactivation in tumorigenesis. International Journal of Molecular Sciences 21 (13) , 4580. 10.3390/ijms21134580

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Abstract

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

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Biosciences
Publisher:	MDPI
ISSN:	1422-0067
Date of First Compliant Deposit:	13 July 2020
Date of Acceptance:	18 June 2020
Last Modified:	06 May 2023 11:55
URI:	https://orca.cardiff.ac.uk/id/eprint/133397

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