Fig. 4

Summary of deregulated phase separations in cancer. A RTK granule formations activate RTK/MAPK signaling pathways to promote tumor proliferation. B DDX21phase separation activates MCM5, facilitating EMT signaling and modulating metastasis of colon cancer. C LLPS of 53BP1 diminish downstream targets of p53 to evade growth suppressions. D The accumulation of 53BP1 in the nuclear foci is enhanced after DNA damage, activating p53 and regulating cellular senescence. E SUMO ALT-associated PML bodies on the telomeres facilitate the replicative immortality of cancer cells. F Nuclear condensates (nYACs) generated through the LLPS of YTHDC1 (binding with m6A-mRNA) are significantly increased in AML cells. G Mutations in the FERM domain of NF2 (NF2m) robustly inhibited STING-initiated antitumor immunity by forming NF2m-IRF3 condensates. H PML nuclear bodies (NBs) serve as comprehensive ROS sensors associated with antioxidative pathways. I EBNA2 becomes part of BMCs and regulates EBV gene transcriptions. J BRD4 forms condensates with SEs to regulate angiogenesis. K NUP98-HOXA9 fusion proteins attenuate aberrant chromatin organizations. L m⁶A-modified androgen receptor (AR) mRNA phase separated with YTHDF3 responds to AR pathway inhibition (ARPI) stress in prostate cancers. M LLPS of GIRGL-CAPRIN1-GLS1 mRNA suppresses GLS1 translation and adapts to an adverse glutamine-deficient environment. N icFSP1 induces FSP1 condensates to trigger ferroptosis in the dedifferentiation of cancer cells