Table 3 Posttranslational modification of ferroptosis by acetylation in cancer
Cancer | Modification | Targets | Enzyme | Biological functions | Ref |
|---|---|---|---|---|---|
NSCLC | Acetylation | p53 | CBP/p300 | Acetylation is crucial for p53-mediated ferroptosis and tumor suppression. | |
NSCLC | Acetylation | p53 | - | p53 inhibits cystine uptake and sensitizes cells to ferroptosis by repressing expression of SLC7A11. Notably, p53,3KR an acetylation-defective mutant that fails to induce cell-cycle arrest, senescence and apoptosis, fully retains the ability to regulate SLC7A11 expression and induce ferroptosis upon ROS-induced stress. | |
NSCLC | Acetylation | p53 | - | GINS4 negatively regulate ferroptosis in LUAD. GINS4 suppressed p53-mediated ferroptosis through stabilizing p53 via activate snail that antagonized the acetylation of p53(K351). | |
HCC | Acetylation | β-OHB | - | HMGCL increased H3K9 acetylation through β-OHB and promoting the expression of DPP4 in a dose-dependent manner, leading to HCC cells vulnerability to erastin- and sorafenib-induced ferroptosis. | |
Glioma | Acetylation | STAT3 | KAT6B | KAT6B contributes to glioma progression by repressing ferroptosis via epigenetically inducing STAT3. | |
Osteosarcoma | Acetylation | p53 | mTOR inhibition acts as an unexpected checkpoint in p53-mediated tumor suppression. | ||
CRC | Acetylation | FSP1 | NAT10 | NAT10 promotes colon cancer progression by inhibiting ferroptosis through N4-acetylation and stabilization of FSP1 mRNA. |
