Table 1.
Summary of in vitro studies of dietary polyphenols against oral cancer.
| Compound | Cell line(s) | Treatment dose/duration | Targets/Outcome (Reference) |
|---|---|---|---|
| BTEs | SCC-4 | 10–40 μg/mL, 24 h | Reducing MMP-2 and uPA [30] |
| Cranberry polyphenols | KB and CAL27 | 200 µg/mL, 48 h | Inhibiting oral cancer cells [31] |
| CG and other TPs | S-G, CAL27, and HSG | 25–200 µM, up to 72 h | Inducing cell death and inhibiting proliferation [29] |
| DMF | SCC-9 | 0.1–100 µM, up to 48 h | Inhibiting CYP1B1/1A1 function [32] |
| ECG and other TPs | HSC-2 and HGF-2 | 50–500 µM, up to 72 h | Inhibiting cell proliferation and inducing apoptosis [33] |
| EGCG | CAL-27 | 25–100 μM, up to 48 h | Suppressing p-EGFR and MMP-2 [34] |
| EGCG | SCC-9 | 5–20 µM, up to 24 h | Reducing expressions of MMP-2, MMP-9, uPA, p-FAK, Src, snail-1, and vimentin [35] |
| EGCG | Tu177, Tu212, Tu686 , and 686LN | 30 µM, up to 72 h | Inducing cell cycle arrest and apoptosis via p53 [36] |
| EGCG | HSC3, HSC4, SCC9, SCC25 | 5–50 µM, up to 5 days | Enhancing RECK expression, inhibiting MMP-2 and MMP-9 expression [37] |
| EGCG | OC2 | 5–60 µM, 24 h | Inhibiting cell invasion and migration [38] |
| EGCG | OSC2, G6, S2, and S5 | 50 µM, up to 72 h | Regulating p21WAF1, p57 modulating epithelial cell differentiation, or apoptosis [39,40] |
| EGCG | OECM-1 | 1–20 µM, 24 h | Inhibiting APP expression [26] |
| EGCG | NS-SV-AC, NSSV, OSC-2, and OSC-4 | 12.5–50 µM, 24 h | Protecting cells from chemical or irradiation-induced damage [41] |
| EGCG and curcumin | MSK Leuk1 | 50 µM, 5 days | Cell growth [27] |
| EGCG, ECG, EGC, resveratrol, and quercetin | SCC-25 | 50–200 µM, up to 72 h | Cell growth [42,43] |
| GTE and EGCG | CAL-27, SCC-25, and KB | 50-200 µM, up to 72 h | Inhibiting cell growth via EGFR and Notch signaling [44] |
| Polyphenon-E and Polyphenon-B | CAL-27 | 25–400 µg/mL, 24 h | Inducting ROS generation and Bcl-2/Bax-mediated apoptosis [45] |
| GTPs and EGCG | OSC2 | 50–200 µM, up to 72 h | Inducing apoptosis, inhibiting cell growth [46,47,48] |
| Methoxylated flavones | SCC-9 | 25 µM, 24 h | Inhibiting CYP1B1 mRNA expression [49] |
| MT | SCC-61 and OSCC-3 | 0.05–1000 µg/mL, 48 h | Inhibiting oral cancer proliferation [50] |
| 150 of natural and synthetic polyphenols | HSC-2, HSG | Various, up to 48 h | Cytotoxic activity [51,52] |
| Quercetin | SCC-9 cells | 0–200 µM, up to 72 h | Inducing cell death [53] |
| Quercetin, resveratrol, and ellagic acid | Oral tissue | 25 µM, 24 h | Inhibiting BaP-DNA binding and oxidization [54] |
| Sasa senanensis Rehder leaves extracts | HSC-2 | 0.22% and 0.18%, 24 h | Protecting cells from ultraviolet -induced injury [55] |
| TF-2A and TF-2B | HSC-2 and CAL27 | 100–500 µM, up to 24 h | Prooxidant action [56,57] |
| TPs | Tca8113 | 25–200 µM, up to 72 h | Inhibiting cell proliferation and hTERT expression [58,59] |
| Tea extracts and EGCG | CAL27, HSC-2, HSG, S-G, GN56, and HGF-1 | 0–200 µg/mL, up to 72 h | Oxidative stress-induced cell death [28] |
| TPs and EGCG | KB-A-1 | 0.2 µg/mL, 24 h | Enhancing intracellular concentration of DOX and modulating MDR [60] |