Table 1.

Role of prooxidant effects in the anticancer activity of EGCG based on cell culture studies.

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]