mRNA sequencing from mouse primary liver tumors and non-tumor livers with RSK2 inactivation in different oncogenic contexts
In order to investigate the tumor suppressor role of RSK2 in the liver, we generated three mouse models combining RSK2 ubiquitous and constitutive inactivation with an additional genetic alteration using transgenic mice and liver-specific chemical carcinogens. In the first two models, RSK2 inactivation was combined either with Axin1 bi-allelic inactivation induced in the liver at 6 weeks of age using the Cre/loxP system, or with ß-catenin activation induced by diethylnitrosamine (DEN) administrated at 6 weeks of age, followed by continuous phenobarbital (PB) treatment. The third model was generated by treating juvenile mice with DEN alone, which is known to induce liver tumors with BRAF activating mutations in the C57BL/6J background. mRNA sequencing was performed from liver tumors developed in the three mouse models and from non-tumor livers of 6 weeks old mice from the model of RSK2 and/or AXIN1 inactivation.