Table 2.
Summary of the use of EGCG in different cell lines.
| Flavonoid | Cell Line | Dose | Results | Reference |
|---|---|---|---|---|
| EGCG and pEGCG | MCF-7 and MDA-MB-231 breast cancer cell lines. MCF10A cell line (normal control) | Apoptosis induction and hTERT inhibition: EGCG (40 μmol/L) and pEGCG (20 μmol/L) Inhibition of cell proliferation: EGCG (60 μmol/L) pEGCG (40 μmol/L) |
pEGCG demonstrated higher potency compared to EGCG in the inhibition of cell proliferation and apoptosis induction in breast cancer cell lines. Inhibition of hTERT was also shown in both cell lines. |
[55] |
| EGCG | T47D breast cancer cells | 80 µM | A significant decrease in hTERT gene expression causing apoptosis was observed. | [56] |
| MST-312 (derivative of EGCG) | MCF-7 and MDA-MB-231 breast cancer cell lines | 0–10 µM | Reduction in telomerase activity, growth arrest, and induction of telomere dysfunction was observed in both cell lines, while reduced expression of TRF2 (telomere protective protein) in MDA-MB-231 cells. | [57] |
| MST-312 | APL cells | 0.5,1, and 2 µM | Caspase mediated apoptosis, arrest in G2/M-phase of the cell cycle of APL cells. Along with telomerase inhibitory activity, NF-κB activity was also suppressed. Additionally, hTERT, Bcl-2, survivin, Mcl-1, and c-myc genes were downregulated. |
[59] |
| EGCG | SCLC cells (H69 and H69VP) | 70 µM | 50–60% Reduction in telomerase, 50 and 70% reduction in caspase 3 and 9, respectively, and block in the S-phase of the cell cycle was observed. | [60] |
| EGCG | Eca109 and Ec9706 | 100, 200, or 300 mg/L | EGCG produced apoptosis, reduced the mitochondrial membrane potential, and raised the expression of caspase-3 and led to the inhibition of telomerase. | [61] |
| EGCG | Nasopharyngeal carcinoma cell line CNE2 | 100, 200 µg/mL, | Prevented CNE2 cells from proliferating, caused cell cycle block, apoptosis of the cells was promoted, and downregulation of the mRNA and protein expression of hTERT as well as c-Myc protein. | [62] |
| EGCG | HEC-18, HEC-18T, HEN-18, HEN-18S | 100 µM | Growth inhibition greater than 90% and induction of apoptosis was observed in HEC-18 and HEN-18. Telomerase was inhibited in all 4 cells. |
[63] |
| EGCG | OMC-4 and TMCC-1 | 50 and 100 µM | Growth and telomerase inhibition, induction of apoptosis and pKi-67 suppression was observed in both cell lines. | [64] |
| EGCG and Retinoic Acid | HeLa and TMCC-1 | EGCG: 100 µM RA: 1 µM |
Combination treatment caused inhibition of telomerase, induction of apoptosis and prevented cell proliferation. | [65] |
| EGCG and Sulforaphane | SKOV3-ip1 and SKOV3TR-ip2 cells | 20 mmol/L EGCG and 10 mmol/L SFN | Combination treatment led to ovarian cancer cell inhibition, arrest in cell cycle phase G2/M and S, induction of apoptosis and DNA damage, reduction in hTERT and DNA methyltransferase 1 | [66] |
| EGCG and EGC | H1299, OECM-1, SAS, WRO, SK-Hep-1, and Hep-3B cells | 10–40 µM | EGCG and EGC caused apoptosis and suppressed hTERT mRNA and promoter activity. | [67] |
| EGCG, Cisplatin, and Tamoxifen | 1321N1 and U87-MG cells | EGCG (100 µM) Cisplatin (up to 50 µM) Tamoxifen (up to 20 µM) |
Telomerase suppression activity was observed in both glioma cell lines when used in combination. | [68] |