Integrated multi-omics analysis of RB-loss identifies widespread cellular programming and synthetic weaknesses.

ABSTRACT: Inactivation of RB is one of the hallmarks of cancer, however gaps remain in our understanding of how RB-loss changes human cells. Here we show that pRB-depletion results in cellular reprogramming, we quantitatively measured how RB-depletion altered the transcriptional, proteomic and metabolic output of non-tumorigenic RPE1 human cells. These profiles identified widespread changes in metabolic and cell stress response factors previously linked to E2F function. In addition, we find a number of additional pathways that are sensitive to RB-depletion that are not E2F-regulated that may represent compensatory mechanisms to support the growth of RB-depleted cells. To determine whether these molecular changes are also present in RB1^-/- tumors, we compared these results to Retinoblastom

SUBMITTER: Rajasekaran S 

PROVIDER: S-EPMC8371045 | biostudies-literature | 2021 Aug

REPOSITORIES: biostudies-literature