Table 1 Main mechanisms of LLPS in lung cancer
From: New insights into the important roles of phase seperation in the targeted therapy of lung cancer
Types | Representative substance | Mechanisms | References |
|---|---|---|---|
Tumor suppressor protein | P53, PTEN | Mutations in them can disrupt the formation of their liquid droplets, leading to impaired DNA repair and increased genomic instability | |
NONO | Â | Function as sites of DNA repair and signal transduction,influence the positioning of EGFR NONO promotes TAZ LLPS | [19] |
DUB | USP42 | Govern the phase separation of PLRG1 to promote tumorigenesis | [21] |
Non-membranous compartment | Stress granule | Improve survival advantages and chemotherapy resistance of malignant tumor cells | [33] |
Phosphatase | SHP2 | SHP2mut induces strong LLPS to recruit SHP2WT and promote ERK activation | [26] |
Lysine methyltransferase | EZH2 | Myristoylation-mediated phase separation of EZH2 activates STAT3 signaling and promotes lung tumor growth | [27] |
| Â | YAP, TAZ | Undergo LLPS and accumulate in the nucleus to drive oncogenic genes | [28] |
RTK | ALK | LLPS of EML4-ALK actives several signalings in lung cancer | [29] |