Table 2.
Role of EGCG in cancer prevention through based on in vitro study.
| Cancer Types | Study Type | Finding of the Study | Refs. |
|---|---|---|---|
| Cervix cancer | In vitro | EGCG with eugenol amrogentin greatly inhibit the cellular proliferation and colony formation | [44] |
| Cervix cancer | In vitro | EGCG treatment causes down regulation of genes involved in the stimulation of proliferation and motility and invasion processes. | [46] |
| Breast cancer | In vitro | EGCG reduced breast cancer cell growth in a concentration- and time dependent manner | [48] |
| Breast cancer | In vitro | Epigallocatechin gallate powerfully inhibited the growth of cancer stem/progenitor cells. | [49] |
| Breast cancer | In vitro | Protein expression of HIF-1α and VEGF dropped in cancer cells pre-treated with increasing concentrations of | [51] |
| Ovarian cancer | In vitro | EGCG improved the toxicity of cisplatin and epigallocatechin-3-gallate increased cisplatin strength | [52] |
| Ovarian cancer | In vitro | EGCG plays an important role in decreasing ovarian cancer cell growth. Correspondingly, Epigallocatechin gallate showed growth inhibitory effects in each cell line in a dose-dependent approach and induced apoptosis and cell cycle arrest | [56] |
| Ovarian cancer | In vitro | Epigallocatechin-3-gallate causes a substantial task in decreasing cancer cell growth, showed dose dependent growth inhibitory effects | [57] |
| Endometrial cancer | In vitro | EGCG caused the arrest of cells in the G0/G1 phase of the cell cycle | [62] |
| Endometrial cancer | In vitro | EGCG was established to inhibit proliferation of adenocarcinoma cells | [63] |
| Pancreatic cancer | In vitro | EGCG decreased pancreatic cancer cell migration, growth and invasion | [67] |
| Pancreatic cancer | In vitro | EGCG reduced pancreatic cancer cell growth in a concentration-dependent manner | [68] |
| Pancreatic cancer | In vitro | The synergistic activity was credited to the cell cycle arrest and the induction of the reactive oxygen species-dependent mitochondria mediated apoptosis | [70] |
| Pancreatic cancer | In vitro | EGCG caused growth arrest at G1 stage of cell cycle, and induced apoptosis | [72] |
| Gastric cancer | In vitro | EGCG was accomplished to inhibit vascular endothelial growth factor secretion and expression | [74] |
| Gastric cancer | In vitro | EGCG significantly inhibited proliferation and increased apoptosis of cancer cells in vitro. | [75] |
| Gastric cancer | In vitro | EGCG meaningfully promoted apoptosis and inhibited the proliferation | [77] |
| Gastric cancer | In vitro | EGCG treatment reduced vascular endothelial growth factor protein level | [78] |
| Gastric cancer | In vitro | Microvessel density in tumor tissues receiving epigallocatechin-3-gallate treatment was also evidently reduced and markedly reduced VEGF protein level | [79] |
| Liver tumour | In vitro | The epigallocatechin gallate reduced hypoxia-incited apoptosis in HepG2 cells as well as enhanced cell survival | [82] |
| Liver cancer | In vitro | Epigallocatechin gallate reduced expression of MMP-9, syndecan-1 and FGF-2 | [83] |
| Colorectal cancer | In vitro | Epigallocatechin gallate and sodium butyrate combination treatment induced apoptosis and cell cycle arrest | [85] |
| Colon cancer | In vitro | EGCG-induced downregulation of epidermal growth factor receptor cancer cells | [86] |
| Colon cancer | In vitro | Both Epigallocatechin-3-gallate and Poly E initiated a decrease in the phosphorylated forms of EGFR | [87] |
| Bile duct cancer | In vitro | JAK/STAT pathway activation through pro-inflammatory cytokine in cancer cells was decreased via pre-treatment with quercetin and epigallocatechin-3-gallate | [91] |
| Bile duct cancer | In vitro | The combination of vorinostat and epigallocatechin-3-gallate revealed synergistic growth inhibitory effects and caused induction of apoptosis in tumor cells. | [92] |
| Renal Cell Carcinoma | In vitro | Epigallocatechin-3-gallate inhibits growth and induces apoptosis | [94] |
| Renal Cell Carcinoma | In vitro | EGCG showed potentiality to inhibit the proliferation, and induce apoptosis | [95] |
| Renal Cell Carcinoma | In vitro | EGCG treatment provoked important upregulation of Cx32 in cancer cells | [97] |
| Prostate Cancer | In vitro | EGCG induces apoptosis through triggering caspase and preventing the expression of Bcl-2 | [99] |
| Prostate Cancer | In vitro | Epigallocatechin-3-gallate demonstrated low inhibitory effect on cancer cell proliferation | [100] |
| Prostate Cancer | In vitro | EGCG showed anticancer effects and it was proved that epigallocatechin-3-gallate inhibited cancer cell proliferation | [102] |
| Urinary bladder cancer | In vitro | Treatment of EGCG caused in important inhibition of cell proliferation via induction of apoptosis and inhibited cancer cell migration | [104] |
| Urinary bladder cancer | In vitro | Epigallocatechin-3-gallate increased growth inhibition in a dose- and time-dependent manner | [105] |
| Leukemia | In vitro | Proliferation and cell cycle progression of cancer cells treated with epigallocatechin-3-gallate were inhibited | [109] |
| Leukemia | In vitro | Epigallocatechin-3-gallate treatment induced apoptosis and increased the levels of Bax protein expression | [111] |
| Leukemia | In vitro | EGCG showed higher growth suppression and induced apoptosis demonstrated by nuclei fragmentation and nuclear fragmentation | [113] |
| Lymphoma | In vitro | EGCG induced growth inhibition and apoptosis in a dose- and time-dependent way | [114] |
| Lymphoma | In vitro | Epigallocatechin-3-gallate were able to inhibit the growth of malignancy cell lines | [115] |
| Lymphoma | In vitro | EGCG caused induction of cell death and reactive oxygen species generation | [116] |
| Head and neck cancer | In vitro | EGCG inhibits the self-renewal capacity and reduces the expression of stem cell markers | [118] |
| Head and neck cancer | In vitro | EGCG induces apoptosis of cancer cells via regulating Bim and Bcl-2 | [119] |
| Head and neck cancer | In vitro | Combined treatment with erlotinib and EGCG inhibited the protein level of p65 subunit of nuclear factor-kappaB | [120] |
| Oral cancer | In vitro | EGCG inhibited cell viability in a time- and concentration-dependent manner | [122] |
| Oral cancer | In vitro | Epigallocatechin-3-gallate in inhibiting HGF-induced tumor growth and invasion | [124] |
| Oral cancer | In vitro | EGCG caused an inhibitory effect on cell migration, motility, spread, and adhesion | [125] |
| Oesophagus cancer | In vitro | Epigallocatechin-3-gallate considerably reduced the invasion and viability capacity of cancer cells | [127] |
| Oesophagus cancer | In vitro | Epigallocatechin-3-gallate inhibited proliferation of cancer cells | [128] |
| Lymphoma | In vitro | Vorinostat alone or in combination with epigallocatechin-3-gallate imparts anti-proliferative effects | [130] |
| Lymphoma | In vitro | EGCG-induced inhibition of tumor cell proliferation | [132] |
| Lung cancer | In vitro | EGCG decrease the expression of both Axl and Tyro 3 receptor tyrosine kinases | [139] |
| Myeloma | In vitro | The treatment of the cancer cell line with epigallocatechin-3-gallate inhibits cell proliferation as well induces apoptosis | [141] |
| Myeloma | In vitro | EGCG inhibited the effect of endothelial cell migration induced and the numbers of migrated cells and numbers of migrated cells | [142] |
| Osteosarcoma | In vitro | EGCG has an anticancer effect on cancer cells | [144] |
| Osteosarcoma | In vitro | EGCG showed role in the suppression of proliferation of cancer cells in a concentration-dependent and time-dependent manner | [145] |
| Brain tumor | In vitro | EGCG induced apoptosis in glioma cells. | [147] |
| Brain tumor | In vitro | EGCG treatment leads to a decrease in cell viability and the S-phase cell fraction | [149] |
| Thyroid cancer | In vitro | EGCG decreased the migration and invasion, | [151] |
| Thyroid cancer | In vitro | EGCG considerably suppresses invasion and migration in anaplastic cancer cells | [152] |
| Retinoblastoma | In vitro | EGCG treatment of cancer cells resulted in a dose- and time-dependent decrease in the total pRb | [154] |