Table 1.
Oxysterol-circadian factors influencing HCC development.
| Factor | Notes | Proposed function | References |
|---|---|---|---|
| Oxysterols | Increased in serum of NAFLD, HCV infected patients | Potential biomarkers | (60, 61) |
| Treatment of HepG2 | Cytotoxicity | (62) | |
| 25-hydrohycholesterol | Treatment of rat hepatoma cells | Pro-apoptotic | (62, 63) |
| 25-hydroxycholesterol and OSBPL8 | Treatment and overexpression in HepG2 | Pro-apoptotic | |
| OSBPL8 | Downregulation in Huh7 and HepG2 | Pro-proliferative | (62) |
| Overexpression in HCC cell line | Pro-apoptotic | (64) | |
| LXR | Lower expression in HCC tumors | Lower post-operative survival rate | (65) |
| Activity | Anti-proliferative via SOCS3 | (66) | |
| FXR | Lower expression and activity in HCC tumors | Association with multiple malignant characteristics | (67–72) |
| Overexpression in HCC cell lines | Anti-proliferative, suppressed tumor growth in nude mice | (69) | |
| Downregulation in HCC cell lines | Pro-proliferative, increased migration and invasion, accelerated tumor growth in nude mice | (70) | |
| SREBP1 | Increased expression in HCC cell line | Required for tumor proliferation | (73) |
| CLOCK (NPAS2) | Increased expression in HCC tumors | (74) | |
| SNPs | Associated with increased risk for HCC, survival of TACE treated patients | (75) | |
| PER3 | SNP | Association with survival | (76) |
| PER2 | Knockout mice | Higher diethylnitrosamine induced carcinogenesis | (77) |
| Chronic circadian disruption | Spontaneous hepatocarcinogenesis in mice | Metabolic disruption, CAR activation | (77–79) |
| TIMELESS | HepG2 | Oncogenic | (80) |