|
Cell lines | EGCG concentration | Time | Biological effects | References |
|
Bladder cancer | | | | |
NBT-II | 10-40 μM | 24-72 h | Induced early apoptosis through DNA damage | [18] |
Breast cancer | | | | |
MCF-7 | 10-50 μg/mL | 48 h | Induced cell growth inhibition and apoptosis by downregulating survivin expression via suppressing the AKT pathway and activating caspase-9 | [19] |
MCF-7 | 10-400 μM | 6 h | Induced apoptosis at low doses via activation of JNK, caspase-9, and caspase-3, while inducing necrosis at high doses, which is related to differences in ROS generation and ATP levels | [20] |
Cervical cancer |
HeLa | 50 μM | 24 and 48 h | Increased cell death through DNA damage | [21] |
HeLa | 25-200 μM | 1 h | Induced cell death through generation of ROS and inactivation of Trx/TrxR | [22] |
Colon cancer |
HCT116 | 50-100 μM | 24 h | Induced apoptosis through induction of ROS and epigenetic modulation of apoptosis-related gene expression | [23] |
HT-29 | 25-250 μM | 36 h | Induced apoptotic cell death via activating the JNK pathway, accompanying mitochondrial transmembrane potential transition and cytochrome c release; IC50 was ~100 μM | [24] |
Endometrial carcinoma |
Ishikawa | 25-150 μM | 48 h | Induced apoptosis via ROS generation and p38 MAP kinase activation; IC50 was 132 μM | [25] |
Esophageal cancer |
KYSE 150 | 20 μM | 8 h | Inactivated EGFR by superoxide generated from autooxidation of EGCG | [26] |
Lung cancer |
H661 and H1299 | 20-100 μM | 48 h | Displayed strong growth inhibitory effects against lung tumor cell lines; IC50 was 20 μM | [27] |
H1299 | 10-50 μM | 24 h | Inhibited cell growth through induction of ROS; IC50 was 20 μM | [28] |
Lymphoblastic leukemia |
Jurkat | 12.5-50 μM | 6 h | Induced apoptosis via H2O2 production and hydroxyl radical formation | [29] |
Myeloma |
IM9, RPMI8226, and U266 | 20-100 μM | 24-72 h | Induced apoptosis by modifying the redox system | [30] |
Oral cancer |
SCC-25 and SCC-9 | 100 μM | 1-6 h | Reduced cell viability by inducing mitochondria-localized ROS and decreasing SIRT3 expression | [31] |
Ovarian cancer |
SKOV-3 | 20-50 μg/mL | 2 d | Inhibited cell proliferation and induced apoptosis by inhibiting cell cycle arrest and inducing DNA damage | [32] |
Pancreatic cancer |
PANC-1 | 20-60 μM | 12 h | Induced apoptosis through generation of ROS, as well as caspase-3 and caspase-9 activation | [33] |
MIA PaCa-2 | 100-200 μM | 24 h | Induced stress signals by damaging mitochondria and ROS-mediated JNK activation | [34] |
Primary effusion lymphoma | | | | |
BCBL-1 and BC-1 | 20 μg/mL | 24 h | Induced apoptosis and autophagy through ROS generation | [35] |
Prostate cancer |
PC3 | 1 and 25 μM | 48 h | Reduced cell survival and increased apoptosis; caused a significant alteration in caspase-9 alternative splicing | [36] |
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