Figure 3 |. Overview of the numerous RB binding partners and transcriptional targets that might mediate its tumour suppressor ability.

Presence of RB (retinoblastoma) might prevent tumour formation by inducing differentiation, controlling cell-cycle arrest, maintaining genomic stability and inducing senescence in response to oncogenic stresses. Furthermore, the absence of RB has been associated with increased angiogenesis and metastasis, although the mediators of these functions are less well understood. Surprisingly, presence of RB has a pro-survival function because of its inhibition of cell death through apoptosis and, potentially, autophagy. This function, shown in green, might be necessary for early tumour cell survival in some contexts. This figure depicts a simplified representation of the potential role of RB in tumour suppression. Each function is illustrated with some of the key protein binding partners and transcriptional targets that might be necessary for the function, but they are not meant to be comprehensive. APAF1, apoptotic peptidase activating factor 1; BNIP3, BCL2-interacting protein 3; CDH1, cadherin 1; DNMT1, DNA methylatransferase 1; HIF1α, hypoxia-induced factor 1α; PCNA, proliferating cell nuclear antigen; VEGF, vascular endothelial growth factor.