Lineage-specific oncogenes drive growth of major forms of human cancer using common downstream mechanisms

Aim of the experiment was to identify changes in protein-protein interactions between proliferating and non-proliferating cells. For this purpose, RKO cells were treated with 20nM Trametinib, HCT116 with 8nM Trametinib, and NCI-H1975 100nM Osimertinib. At these concentrations, the wild type cell lines experience G1 cell cycle arrest, whereas the corresponding PTEN knockout cell lines continue to proliferate. PISA was performed at 2h time point, before the changes in gene expression and cell cycle distribution took place in the matching single-cell transcriptomics analysis, and at 24h where cell cycle arrest had occurred.