PMID- 11833065
OWN - NLM
STAT- MEDLINE
DCOM- 20020503
LR  - 20240324
IS  - 1007-9327 (Print)
IS  - 2219-2840 (Electronic)
IS  - 1007-9327 (Linking)
VI  - 8
IP  - 1
DP  - 2002 Feb
TI  - RRR-alpha-tocopheryl succinate inhibits human gastric cancer SGC-7901 cell growth 
      by inducing apoptosis and DNA synthesis arrest.
PG  - 26-30
AB  - AIM: To investigate the effects of growth inhibition of human gastric cancer 
      SGC-7901 cell with RRR-alpha-tocopheryl succinate (VES), a derivative of natural 
      Vitamin E, via inducing apoptosis and DNA synthesis arrest. METHODS: Human 
      gastric cancer SGC-7901 cells were regularly incubated in the presence of VES at 
      5, 10 and 20mg x L(-1) (VES was dissolved in absolute ethanol and diluted in RPMI 
      1640 complete condition media correspondingly to a final concentration of VES and 
      1 mL x L(-1) ethanol), succinic acid and ethanol equivalents as vehicle (VEH) 
      control and condition media only as untreated (UT) control. Trypan blue dye 
      exclusion analysis and MTT assay were applied to detect the cell proliferation. 
      Cells were pulsed with 37kBq of tritiated thymidine and (3H) TdR uptake was 
      measured to observe DNA synthesis. Apoptotic morphology was observed by electron 
      microscopy and DAPI staining. Flow cytometry and terminal deoxynucleotidyl 
      transferase-mediated dUTP nick end labeling (TUNEL) assay were performed to 
      detect VES-triggered apoptosis. RESULTS: VES inhibited SGC-7901 cell growth in a 
      dose-dependent manner. The growth curve showed suppression by 24.7%, 49.2% and 
      68.7% following 24h of VES treatment at 5, 10 and 20 mg x L(-1), respectively, 
      similar to the findings from MTT assay. DNA synthesis was evidently reduced by 
      35%, 45% and 98% after 24h VES treatment at 20mg x L(-1) and 48 h at 10 and 20mg 
      x L(-1), respectively. VES induced SGC-7901 cells to undergo apoptosis with 
      typically apoptotic characteristics, including morphological changes of chromatin 
      condensation, chromatin crescent formation/margination, nucleus fragmentation and 
      apoptotic body formation, typical apoptotic sub-G1 peak by flow cytometry and 
      increase of apoptotic cells by TUNEL assay in which 90% of cells underwent 
      apoptosis after 48 h of VES treatment at 20 mg x L(-1). CONCLUSION: VES can 
      inhibit human gastric cancer SGC-7901 cell growth by inducing apoptosis and DNA 
      synthesis arrest. Inhibition of SGC-7901 cell growth by VES is dose- and 
      time-dependent. Therefore VES can function as a potent chemotherapeutic agent 
      against human gastric carcinogenesis.
FAU - Wu, Kun
AU  - Wu K
AD  - Department of Nutrition and Food Hygiene, Public Health School, Harbin Medical 
      University, Harbin 150001, Heilongjiang Province,China. wukun@public.hr.hl.cn
FAU - Zhao, Yan
AU  - Zhao Y
FAU - Liu, Bai-He
AU  - Liu BH
FAU - Li, Yao
AU  - Li Y
FAU - Liu, Fang
AU  - Liu F
FAU - Guo, Jian
AU  - Guo J
FAU - Yu, Wei-Ping
AU  - Yu WP
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - World J Gastroenterol
JT  - World journal of gastroenterology
JID - 100883448
RN  - 1406-18-4 (Vitamin E)
RN  - 9007-49-2 (DNA)
RN  - R0ZB2556P8 (Tocopherols)
SB  - IM
MH  - Apoptosis/*drug effects
MH  - Cell Division/drug effects
MH  - DNA/biosynthesis
MH  - Dose-Response Relationship, Drug
MH  - Flow Cytometry
MH  - Humans
MH  - In Situ Nick-End Labeling
MH  - *Stomach Neoplasms
MH  - Tocopherols
MH  - Tumor Cells, Cultured/cytology/drug effects
MH  - Vitamin E/*analogs & derivatives/*pharmacology
PMC - PMC4656619
EDAT- 2002/02/08 10:00
MHDA- 2002/05/04 10:01
PMCR- 2002/02/15
CRDT- 2002/02/08 10:00
PHST- 2002/02/08 10:00 [pubmed]
PHST- 2002/05/04 10:01 [medline]
PHST- 2002/02/08 10:00 [entrez]
PHST- 2002/02/15 00:00 [pmc-release]
AID - 10.3748/wjg.v8.i1.26 [doi]
PST - ppublish
SO  - World J Gastroenterol. 2002 Feb;8(1):26-30. doi: 10.3748/wjg.v8.i1.26.