Table 2.
ACSL4 in cancers.
| Cancer | Expression | Function | Reference |
|---|---|---|---|
| Breast cancer | ↑ | High expression of ACSL4 promoted tumor aggression and was a prognostic indicator and potential therapeutic target. | [50] |
| Colorectal cancer | ↑ | ACSL4 promoted EMT and metastasis. | [51,52] |
| Gastric Cancer | ↓ | ACSL4 inhibited cell growth, colony formation, and migration. | [53,54] |
| Glioma | ↓ | ACSL4 promoted tumor necrosis, proliferation, migration, and cell self-renewal ability. | [55,56,57,58] |
| Gallbladder Cancer | ↓ | SIRT3 inhibited ACSL4 expression that drives ferroptosis and promotes the activity of epithelial-mesenchymal (EMT) markers and invasiveness | [59] |
| Hepatocellular Cancer | ↑ | ACSL4 promoted the proliferation and metastasis of HCC cells. | [60,61] |
| Lung Cancer | ↓ | ACSL4 suppressed tumor survival and invasiveness and promoted ferroptosis. | [62] |
| Ovarian cancer | ↑ | ACSL4 was a direct target of miR-424-5p which showed inhibition on ferroptosis that serves as a novel tumor suppressor. | [36] |
| Pancreatic Cancer | ↓ | High protein tyrosine phosphatase mitochondria1(PTPMT1) level inhibited ferroptosis by suppressing the expression of ACSL4 and displayed a lower overall survival rate. | [63] |
| Prostate cancer | ↑ | ACSL4 increased cell proliferation, migration, and invasion. | [64,65] |
”↑” represents up-regulated expression and “↓” represents down-regulated expression.