Table 5.
Cancer Cell | Dose/Duration | Findings | Mechanism | Reference |
---|---|---|---|---|
WEHI-3B D (Murine myeloid leukemia), HL-60 (Myeloid leukemia), U937 (Myeloid leukemia) | RE (10 µM equivalent of CA) (48–96 h) | Potentiated following effects of VDA: ↓ cell proliferation ↑ cell cycle arrest ↑ cell differentiation ↑ apoptosis |
↑ G1 phase | [41] |
RAW 264.7 (Murine leukemia; macrophage), HL-60 (Myeloid leukemia), K-562 (Human leukemia) | 0.1%–20% (5–120 h) (1–200 mg/mL) | ↓ cell proliferation IC50 ~18.76 µg/mL and 33.5 µg/mL ↑ cell differentiation ↓ LPS-stimulated (LS) antioxidant activity |
↓ (LS) NO ↑ antioxid-ant activity ↔ basal TNFɑ, IL-1β, iNOS or COX2 ↓ (LS) IL-1β and COX2 |
[29] |
WEHI-3B D (Murine myeloid leukemia) | RE (10 µM equivalent of CA) (48–96 h) | Potentiated following effects of VDA: ↑ cell differentiation ↓ cell viability ↓ cell proliferation |
↓ ROS ↑ antioxid-ant activity ↑ NADP(H)-quinone reductase |
[40] |
K-562 (Human leukemia) | 6.25–50 µg/mL (48 h) | ↓ cell viability IC50 ~12.50 µg/mL | [30] | |
K-562 (Human leukemia), U937 (Myeloid leukemia) | 50 µg/mL (0–96 h) | ↓ cell proliferation | ↓ AKT1 ↑ Rb2 ↔ ERK2 |
[42] |
VDA (vitamin D analogue), LPS (lipopolysaccharide), NO (nitric oxide), TNFα (tumor necrosis factor α), IL-1β (interleukin 1β), iNOS (inducible nitric oxide synthase), COX2 (cyclooxygenase 2), ROS (reactive oxygen species), NADP (nicotinamide adenine dinucleotide phosphate), Rb2 (retinoblastoma-related gene 2).