The publication aims to explain the mechansism of GBM cytotoxicity of Trisenox (As2O3), otherwise an antileukemic drug. As2O3 triggers the autophagy via free radicals and simultaneously inhibits lysosomal CatB, causing apoptotic switch. We can drastically enhance this by inhibiting CatL, which we previously proved to have an antiapoptotic acitivity. This finding needs further confirmation in animal studies before it can be translated to clinics.
In this work we studied how the most abundant stromal cells in glioblastoma (GBM), i.e. endothelial cells and macrophages influence the phenotype of GBM cells. Stromal cells did not impact proliferation of tumour cells, but enhanced their invasion and reduced the triggered apoptotic response. On the other hands, GBM cells stimulate proliferation of stromal cells. We concluded that stromal cells create then environment, which facilitates and contributes to the development of GBM. GBM cells stimulate the growth of these cells thereby assuring a better environment for tumour progression.