Figure 1.

Targeting cellular senescence in cancer. Senescent cells induced by oncogenic stress exhibit proliferation arrest with metabolic reprogramming. Oncogene-induced senescence (OIS) is often accompanied by the activation of signaling pathways such as BRAF/MEK/ERK and PI3K/AKT/mTOR. OIS is usually featured with increased SA-β-gal activation; the accumulation of p53 and/or RB; the activation of DDR and autophagy; and SASP. The senescent phenotype could be different and is dependent on temporal, spatial and genetic contexts. Senescent cells could be eradicated by the induction of apoptosis by pan-BCL inhibitors such as ABT-263 or by the immune surveillance system. In addition, compounds such as metformin that are able to block SASP can eliminate the deleterious effect of cellular senescence.