Editorial Volume 15, Issue 10 pp 3896—3898

Figure 1. BET-1/BRD4’s role in regulation of actin stability impacts aging and age-related diseases. Left: In C. elegans, BET-1 can induce transcription of actin regulatory genes and promote stress resilience to promote longevity. While increased actin stability and stress resilience are both correlated with increased bet-1 expression, whether increased actin stability directly impacts stress resilience or vice versa are still unknown. Right: In mammalian cells increased BRD4 activity can be detrimental by promoting senescent cell survival and increased cancer aggression. Inhibition of BRD4 activity results in destabilization of F-actin filaments, which can prevent angiogenesis and metastasis of cancer cells and is correlated with decreased senescent cell survival, although whether the decreased stability of actin is the direct cause of senescent cell death is still unknown. These data suggest that BRD4 can be a viable therapeutic target both for its anti-cancer and senolytic properties.