Computational Modelling of Aquaporin Co-regulation in Cancer

TL;DR

This paper presents a qualitative computational model of aquaporin regulation in cancer cells, linking key aquaporins to cancer phenotypes through dysregulated signaling pathways, and offers novel predictions for experimental validation.

Contribution

It introduces a new qualitative network model that integrates multiple signaling pathways affecting aquaporin regulation in cancer, reconciling conflicting phenotypic data.

Findings

Model reproduces experimental results qualitatively

Suggests molecular mechanisms for phenotype regulation

Provides novel predictions for experimental testing

Abstract

A computational model of aquaporin regulation in cancer cells has been constructed as a Qualitative Network in the software BioModelAnalyzer (BMA). The model connects some important aquaporins expressed in human cancer to common phenotypes via a number of fundamental, dysregulated signalling pathways. Based on over 60 publications, this model can not only reproduce the results reported in a discrete, qualitative manner, but also reconcile the seemingly incompatible phenotype with research consensus by suggesting molecular mechanisms accountable for it. Novel predictions have also been made by mimicking real-life experiments in the model.