PMID- 21167021
OWN - NLM
STAT- MEDLINE
DCOM- 20110318
LR  - 20220316
IS  - 1756-9966 (Electronic)
IS  - 0392-9078 (Print)
IS  - 0392-9078 (Linking)
VI  - 29
IP  - 1
DP  - 2010 Dec 17
TI  - Catechin hydrate suppresses MCF-7 proliferation through TP53/Caspase-mediated 
      apoptosis.
PG  - 167
LID - 10.1186/1756-9966-29-167 [doi]
AB  - Catechin hydrate (CH), a strong antioxidant that scavenges radicals, is a 
      phenolic compound that is extracted from plants and is present in natural food 
      and drinks, such as green tea and red wine. CH possesses anticancer potential. 
      The mechanism of action of many anticancer drugs is based on their ability to 
      induce apoptosis. In this study, I sought to characterize the downstream 
      apoptotic genes targeted by CH in MCF-7 human breast cancer cells. CH effectively 
      kills MCF-7 cells through induction of apoptosis. Apoptosis was confirmed by 
      terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and 
      real-time PCR assays. Cells were exposed to 150 mug/ml CH and 300 mug/mL CH for 24 
      hours, which resulted in 40.7% and 41.16% apoptotic cells, respectively. 
      Moreover, a 48-hour exposure to 150 mug/ml CH and 300 mug/ml CH resulted in 43.73% 
      and 52.95% apoptotic cells, respectively. Interestingly, after 72 hours of 
      exposure to both concentrations of CH, almost 100% of cells lost their integrity. 
      These results were further confirmed by the increased expression of caspase-3,-8, 
      and -9 and TP53 in a time-dependent and dose-dependent manner, as determined by 
      real-time quantitative PCR. In summary, the induction of apoptosis by CH is 
      affected by its ability to increase the expression of pro-apoptotic genes such as 
      caspase-3, -8, and -9 and TP53.
FAU - Alshatwi, Ali A
AU  - Alshatwi AA
AD  - Molecular Cancer Biology Research Lab, Dept, of Food Science and Nutrition, 
      College of Agriculture and Food Sciences, King Saud University, Saudi Arabia. 
      alialshatwi@gmail.com
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20101217
PL  - England
TA  - J Exp Clin Cancer Res
JT  - Journal of experimental & clinical cancer research : CR
JID - 8308647
RN  - 0 (Antineoplastic Agents)
RN  - 0 (Antioxidants)
RN  - 0 (Tumor Suppressor Protein p53)
RN  - 8R1V1STN48 (Catechin)
RN  - EC 3.4.22.- (Caspases)
SB  - IM
MH  - Antineoplastic Agents/*pharmacology
MH  - Antioxidants/pharmacology
MH  - Apoptosis/*drug effects
MH  - Breast Neoplasms/*metabolism
MH  - Caspases/drug effects/metabolism
MH  - Catechin/*pharmacology
MH  - Cell Line, Tumor
MH  - Cell Proliferation/*drug effects
MH  - Female
MH  - Humans
MH  - In Situ Nick-End Labeling
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Signal Transduction/drug effects
MH  - Tumor Suppressor Protein p53/drug effects/metabolism
PMC - PMC3019143
EDAT- 2010/12/21 06:00
MHDA- 2011/03/19 06:00
PMCR- 2010/12/17
CRDT- 2010/12/21 06:00
PHST- 2010/09/06 00:00 [received]
PHST- 2010/12/17 00:00 [accepted]
PHST- 2010/12/21 06:00 [entrez]
PHST- 2010/12/21 06:00 [pubmed]
PHST- 2011/03/19 06:00 [medline]
PHST- 2010/12/17 00:00 [pmc-release]
AID - 1756-9966-29-167 [pii]
AID - 10.1186/1756-9966-29-167 [doi]
PST - epublish
SO  - J Exp Clin Cancer Res. 2010 Dec 17;29(1):167. doi: 10.1186/1756-9966-29-167.