Table 1.
Effects of Resveratrol against Cervical Cancer: in vitro studies.
| Cell | Resveratrol Concentration/Duration | Effect | Reference |
|---|---|---|---|
| HeLa, SiHa cervical cancer cells | 10, 25 µM 1–8 days |
Increased effects of IR ↓cell growth ↓cell survival ↑cell cycle arrest (S phase) ↓COX-1 activity |
[36] |
| HeLa cells | 50 & 75 µM 24 h |
↓PMA effects ↓MMP-9 mRNA, protein & activity ↓JNK ↓PKC δ ↓AP-1 ↓NFkB |
[37] |
| HeLa cervical cancer cells | 5, 25 & 50 µM 24–48 h |
↓cell growth Accumulation in the S phase of the cell cycle |
[38] |
|
C-33A and HeLa Expressing HPV E6, E7 |
25, 50 &100 µM 16 h |
↓HIF-1a ↓VEGF |
[39] |
| hHeLa, Cx, SiHa and SKGIIIb cervical cancer cells |
100–400 µM 24–72 h |
↓cell growth ↑autophagy ↑apoptosis ↑LC3-II ↑LMP ↑Cat L ↑Cytochrome C ↑caspase-3 |
[40] |
| SKG-I SKG-II SKG-IIIa Nuz HeLa Cervical cancer cells |
10, 30 & 100 μΜ | ↑autophagy ↑apoptosis ↓drug resistance ↓ATAD3A ↑abrasion of the mitochondrial outer membrane ↑autophagosomes |
[41] |
| HeLa cervical cancer cells | 10, 30 & 100 μΜ 24 h |
↓invasion ↓metastasis ↓MMP9 levels-activity ↓NF κΒ ↓AP-1 |
[42] |
| HeLa cervical cancer cells | 25 μΜ 24, 48 & 72 h |
↓cell proliferation ↑apoptosis ↑caspase-9 ↑caspase-3 ↓mitochondrial membrane potential -JC-1 in monomeric form ↓HDM2 |
[43] |
| C33A (with mutated p53) HeLa(HPV18positive) CaLo(HPV18positive) CaSki(HPV16positive) SiHa(HPV16 positive) |
150–250 µM 48 h |
↓proliferation ↑apoptosis ↓mitochondrial membrane potential ↑mitochondrial and lysosomal permeability ↑p53 levels ↓p65 NF κB levels |
[44] |
| HeLa SiHa cervical cancer cells |
100 μΜ 12–48 h |
↑S-phase cell cycle arrest ↑apoptosis ↓p-STAT3 ↓Notch1/2 ↓Hes1 ↓Wnt2/5a ↓β-catenin ↑PIAS3 |
[45] |
| HeLa cervical cancer cells | 10 & 100 μΜ 24 h |
↓cell viability ↓cell proliferation ↓cell survival ↑GRIM-19 ↓p-STAT3 ↓cyclin B1 ↓VEGF ↓Bcl-2 |
[46] |
| HeLa SiHa C33A cervical cancer cells |
100 μΜ 12, 24, 36 & 48 h |
↓cell growth ↓proliferation ↑apoptosis ↓p-STAT3 ↓survivin ↓c-Myc ↓cyclin D1 ↓VEGF ↑SOCS3 ↑PIAS3 |
[47] |
| cancer stem cells (CSC) from HeLa cultures (HeLa SP) | 137 μM 48–72 h |
↓cell viability ↑apoptosis ↓RAD51 |
[48] |
| HeLa cervical cancer cells | 5–40 µM 24–48 h |
↓cell viability ↓cell migration ↑cell cycle arrest (S phase) ↓viral oncogene E6 ↑p53 levels |
[49] |
| HeLa | 10–80 µM 12–36 h |
↓cell proliferation ↑cell cycle arrest at G1/S phase ↑p53 levels ↑apoptosis |
[50] |
| HeLa | 10–40 µM 24–48 h |
↓cell viability ↓cell proliferation ↑apoptosis ↑caspase-3 ↑caspase-9 ↑Bax ↓Bcl-2 ↓Bcl-XL ↑p53 ↓Cyclin B1 |
[51] |
| HeLa | 0–100 µM 24–96 h |
↓Cell growth ↓Cell viability ↓Proliferation ↓Phospholipid scramblase 1 |
[52] |
| SiHa | 100 µM 24 h |
↓Cell viability ↑Cell cycle arrest in G2/M ↑Apoptosis ↓Survivin mRNA levels ↓Survivin protein levels ↑E-cadherin |
[53] |
| HeLa | 2.5–150 µM 24–48 h |
↓Cell viability ↑Cytotoxicity ↑necrosis |
[54] |
| HeLa |
0–80 µM 48 h |
↓Proliferation ↑Apoptosis ↓p-FOXO3a ↑FOXO3a ↑Bim ↓p-ERK |
[55] |
| HeLa SiHa |
0–40 µM 24 h |
↓Proliferation ↓Wound healing ↓Migration/invasion ↓Metastasis ↑E-cadherin ↓N-cadherin ↓vimentin ↓MMP-3/13 protein levels ↓STAT3 protein levels |
[56] |
| HeLa | 20 µM 24 h |
↓Cell viability ↑Cytotoxicity ↓Glucose uptake ↓NADH/NAD+ ratio ↓Lactate ↑Pyruvate |
[57] |
| W12 | 0–100 µM | ↓Proliferation | [58] |
| HeLa Ca Ski |
5–40 µM 24 h |
↓Proliferation ↑Cell cycle arrest in S phase ↑Apoptosis ↑p16/21/27 ↓CDK4 ↓E2F1 ↓p-pRb1 ↓Bcl-2 mRNA & protein levels ↓Bcl-xL mRNA levels ↑Bax protein levels ↑E6/7 ↑p53 |
[59] |
| HT-3 | 0.16–1.25 µM 0–48 h |
↓Cell viability ↓Cell growth ↓Proliferation ↑Apoptosis |
[60] |
| HeLa | 262.87 µM 24 h |
↓Cell viability ↑Apoptosis ↑mRNA caspases-3/-8/-9 levels ↑NCLX |
[61] |
| HeLa | 20 µM 24 h |
↑Cell cycle arrest in S phase ↓Colony formation ↓EGFR |
[62] |