Journal
BIOESSAYS
Volume 44, Issue 3, Pages -Publisher
WILEY
DOI: 10.1002/bies.202100224
Keywords
autophagy; cell heterogeneity; mathematical model; precision medicine; transduction pathways; YAP1 signalling
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Funding
- UK Dementia Research Institute
- Romanian Ministry of Research, Innovation and Digitization, CNCS/CCCDI-UEFISCDI [PN-III-P1-1.1-PD2019-0733]
- PNCDI-III [POC/448/1/1/127606]
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Autophagy and YAP1-WWTR1/TAZ signaling are tightly linked, with distinct posttranslational modifications dominating these pathways in different cells. The study suggests that understanding these modifications is crucial for developing cell type-specific therapeutic strategies for cancers and other diseases.
Autophagy and YAP1-WWTR1/TAZ signalling are tightly linked in a complex control system of forward and feedback pathways which determine different cellular outcomes in differing cell types at different time-points after perturbations. Here we extend our previous experimental and modelling approaches to consider two possibilities. First, we have performed additional mathematical modelling to explore how the autophagy-YAP1 crosstalk may be controlled by posttranslational modifications of components of the pathways. Second, since analogous contrasting results have also been reported for autophagy as a regulator of other transduction pathways engaged in tumorigenesis (Wnt/beta-catenin, TGF-beta/Smads, NF-kB or XIAP/cIAPs), we have considered if such discrepancies may be explicable through situations involving competing pathways and feedback loops in different cell types, analogous to the autophagy-YAP/TAZ situation. Since distinct posttranslational modifications dominate those pathways in distinct cells, these need to be understood to enable appropriate cell type-specific therapeutic strategies for cancers and other diseases.
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