Table 1.
Anticancer effects of Rosemary Extract (RE). In vitro studies: colon cancer.
| Cancer Cell | Dose/Duration | Findings | Mechanism | Reference |
|---|---|---|---|---|
| CaCo-2 (Colorectal adenocarcinoma) | 0.1–30 µg/mL (3–24 h) | ↓ cell colony formation. Long and short term antioxidant effects | ↓ H2O2-induced DNA strand breaks and oxidative damage. ↓ visible light-induced oxidative damage |
[15] |
| SW480 (Colorectal adenocarcinoma) | 31.25–500 µg/mL (48 h) | ↓ cell proliferation. Cytotoxic above 250 µg/mL. IC50~71.8 µg/mL |
[16] | |
| HT-29 (Colorectal adenocarcinoma) | RE containing 10 µM total polyphenols (72 h) | ↓ cell proliferation ↑ cell cycle arrest ↑ apoptosis |
[17] | |
| HT29 (Colorectal adenocarcinoma) | 1.95–62.5 µg/mL (48 h) 3 RE’s standardized to 25.9%, 36.2%, 42.4% CA | ↓ cell proliferation IC50 > 62.5 µg/mL |
[18] | |
| SW480 (Colorectal adenocarcinoma), HT29 (Colorectal adenocarcinoma) | RE containing 10 µM total polyphenols (48 h) | ↓ cell proliferation SW480 more sensitive ↑ cell cycle arrest |
↑ antioxidant and xenobiotic effects Modulates: Nrf2, ER stress genes, cell cycle, proliferation genes | [19] |
| SW620 (Colorectal adenocarcinoma), DLD-1 (Colorectal adenocarcinoma) | 20–110 µg/mL (24–48 h) | ↓ cell proliferation IC50 36.4 and 34.6 µg/mL Effect on 5-FU sensitive and resistant cells ↑ apoptosis ↓ cell transformation |
Modulates TYMS and TK1. ↑ PARP cleavage |
[20] |
| SW620 (Colorectal adenocarcinoma), DLD-1 (Colorectal adenocarcinoma) | 20–120 µg/mL (48 h) | ↓ cell viability IC50 25 µg/mL |
↑ PARP cleavage. ↑ GCNT3. ↓ miR-15b gene expression |
[21] |
| HT-29 (Colorectal adenocarcinoma), W480 (Colorectal adenocarcinoma), HGUE-C-1 (Colorectal carcinoma) | 1.5–100 µg/mL (24–48 h) | ↓ cell viability | [22] | |
| HCT116 (Colorectal carcinoma), SW480 (Colorectal adenocarcinoma) | 10–100 µg/mL (24 h, 48 h, 72 h) Standardized to 23% CA | ↓ cell viability ↑ apoptosis |
↑ Nrf2 ↑ PERK ↑ sestrin-2 ↑ HO-1 ↑ cleaved-casp 3 |
[23] |
| HT-29 (Colorectal adenocarcinoma) | 30 µg/mL (2–72 h) | ↓ cell proliferation ↑ cell cycle arrest ↑ cholesterol accumulation ↑ ROS accumulation |
↑ UPR ↑ ER-stress ↓ cell cycle genes Altered cholesterol-modulating genes |
[24] |
| HT-29 (Colorectal adenocarcinoma) | 30–70 µg/mL (24 h, 48 h) | ↓ cell proliferation IC50 16.2 µg/mL ↑ necrosis |
↑ Nrf2 pathway ↑ UPR ↑ autophagy |
[25] |
| HT-29 (Colorectal adenocarcinoma) | 30–60 µg/mL (6 h, 24 h) | ↓ cell proliferation ↑ cell cycle arrest |
↑ H2O2 in media ↑ ROS levels ↑ HO-1 and CHOP expression |
[26] |
H2O2 (hydrogen peroxide), 5-FU (fluorouracil), TYMS (thymidylate synthase), TK1 (thymidine kinase 1), PARP (poly ADP ribose polymerase), GCNT3 (glucosaminyl (N-acetyl) transferase 3), miR-15b (microRNA-15b). GI50 (50% growth inhibition), TGI (total growth inhibition), Nrf2 (nuclear factor erythroid 2-related factor 2), casp (caspase), UPR (unfolded protein response), ER (endoplasmic reticulum), HO-1 (heme oxygenase protein-1), CHOP (C/EBP homologous protein).