Table 1.
The effects of green tea catechins on anticancer compounds in anti-tumor activity.
| Anticancer Drugs | Experiment | Effects | Reference |
|---|---|---|---|
| Bleomycin | SiHa cervical cancer cells or uterine cervical cancer cells were treated with tea polyphenol and bleomycin; poly-caspase activity, early apoptosis, and the expression of caspase-3, caspase-8, caspase-9, Bcl-2, and p53 were assessed. | Synergistic increase in antitumor effects. | [10] |
| 5-Fluorouracil (5-FU) | Some cancer cells—such as human SW480, BIU-87, BGC823, and Hep3B—were treated with green tea and 5-FU; the cytotoxicity, cell apoptosis, and proliferation were studied. | Increase in cell apoptosis; synergistic inhibition of cell proliferation; no reduction in antitumor activity. | [15,35] |
| Cisplatin | Cancer cells YCU-N861, YCU-H891, Hep3B, SW480, BIU-87, BGC823, et al. were coadministered cisplatin with tea polypnenols; the cell apoptosis and proliferation were studied. | Synergistic inhibition of cell proliferation; induction of apoptosis. | [20,21,22] |
| Ibuprofen | DU-145 cells were treated with EGCG and ibuprofen; cell death analysis, immunoblotting, RT-PCR analysis, and caspase activity assay were used. | Synergistic effect on the anti-proliferative and pro-apoptotic action. | [23] |
| Tamoxifen | Cancer cells PC-9, MCF-7, and MDA-MB-231were treated with tea polyphenols and tamoxifen; some factors such as EGFR, MMP-2, MMP-9, and EMMPRIN were assessed. | Induction of apoptosis; enhanced expression of apoptotic genes; synergistic increase in antitumor effects. | [24,25,26] |
| Sulindac | PC-9 cancer cells were treated with sulindac and tea polyphenols; gene expression was assessed. | Induction of apoptosis; enhanced expression of apoptotic genes. | [27,28] |
| Bortezomib | Cancer cells 26S and CWR22 were treated with bortezomib and tea polyphenols; cell apoptosis and proliferation were assessed. | Antagonized antitumor activity. | [29,30,31] |
| Celecoxib | A549 and MCF-7 cancer cells were treated with celecoxib and tea polyphenols; the cell activity and gene expression were assessed. | Increased cell apoptosis; enhanced expression of GADD153 gene | [32] |
| Luteolin | Cancer cells H292, A549, H460, and Tu212 were treated with luteolin and EGCG; phosphorylation of p53 was studied. | Induction of caspase-8 and caspase-3 cleavage; increase in cell apoptosis. | [33] |
| Docetaxel | PC-3ML cancer cells were treated with docetaxel and tea polyphenols; hTERT and Bcl-2 were studied. | Increase in the expression of apoptotic genes; reduction in growth rate of cancer cells. | [34] |
| Curcumin | Cancer cells PC-9, A549, NCI-H460, and ER alpha-breast cancer cells were treated with curcumin and tea polyphenols; the cell activity and cell cycle were assessed. | Induction of apoptosis; enhancement of cell cycle arrest at G1 and S/G2 phases. | [36,37,38] |
| Quercetin | Cancer cells PC-3, LNCaP, and CWR22Rv1 were treated with quercetin and tea polyphenols; the cell growth and gene expression were assessed. | Synergistic expression of androgen receptor; inhibition of cancer cell growth. | [39,40] |
| Paclitaxel | PC-3ML cancer cells were treated with paclitaxel and tea polyphenols; the cell growth and apoptotic gene expression were assessed. | Increase in the expression of apoptotic genes; reduction in growth rate of cancer cells. | [34,41] |
| Doxorubicin | Cancer cells BEL-7404/DOX, PC-3ML, IBC-10a, and PCa-20a were treated with doxorubicin and tea; the cell proliferation and apoptosis were assessed. | Enhanced sensitivity to doxorubicin; synergistic increase in antitumor effects. | [42] |
| Resveratrol | Cancer cells ALVA-41, PC-3, and MCF-7 were treated with resveratrol and green tea; the cell growth and apoptosis were assessed. | Inhibition of cell growth; induction of apoptosis | [19,43] |
| Sulforaphane | Cancer cells PC-3 AP-1, HT-29, SKOV-ip1, SKOVTR-ip2 were treated with sulforaphane and EGCG; the cell activity and gene expression were assessed. | Diminished induction of cancer cell activity; inhibition of cell viability; increase in apoptosis. | [34,44] |
EGFR (epidermal growth factor receptor); MMP-2, MMP-9 (a family of matrix metalloproteinases); EMMPRIN (extracellular matrix metalloproteinase inducer); hTERT (human telomerase reverse transcriptase); ER (estrogen receptor).