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] |