Atypical cellular responses mediated by intracellular constitutive active TrkB (NTRK2) kinase domains and a solely intracellular NTRK2-fusion oncogene

We report the application of RNA-seq for molecular profiling of cultured, U87MG cells that stably express TrkB. Our data set is based on about 40 million unique reads per sample, in four independent mRNA preparations, for nine different testing conditions. U87MG is a standard human glioblastoma patient derived cell line. It serves as a cellular model for studying molecular characteristics of glioblastoma. We describe in our study the intracellular self-activation of TrkB via Y705 and its role in reducing actin dynamics and cell migraton. With this transcriptome dataset, we wished to highlight key players that are activated after TrkB self-activation. The dataset suggest a transcriptional level reprogramming and switching on of several genes that play a role in modulating immune responses and defense mechanisms, in the modified U87MG cells. Overall design: We generated stable U87MG lines expressing TrkB, an inactive TrkB kinase mutant and a TrkB (NTRK2) gene fusion with SQSTM1 with the help of lentiviral vectors. We switched on the expression of these receptors by treating the cells with Doxycycline for 48 hours, followed by total RNA extraction. RNA seq was done to look at the upregulation and/or downregulation of genes, if any, after TrkB expression.