Fig. 7.

Future prospects of cancer treatment via regulating LLPS. a ARV-825, a novel PROTAC, efficiently degrades BRD4 protein in BL cell lines by linking BRD4 to E3 ubiquitin ligase. b Chloroquine primarily blocks autophagy by impairing autophagosome-lysosomal fusion, thereby upregulate target protein level. c Phosphorylation mediated by activated TORC1 significantly inhibits LLPS and impairs autophagosome prestructure (PAS) formation. d Inhibition of PARylation prevents the formation of DNA damage repair foci. e Cisplatin preferentially concentrates in biomolecule condensates, which can help improve drug efficacy. f Tamoxifen efficiently expels ERα from MED1 condensates via specifically partitioning into these condensates. g The small-molecule compound EPI-001 selectively binds to the IDR of the androgen receptor, thereby slowing the progression of castration-resistant prostate cancer. h EVG can directly target the SRC-1/YAP/TEAD droplets to restrict cancer cell growth in a YAP-dependent manner