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Effects of all-trans-retinoic on human gastric cancer cells BGC-823
Jin Ping Zhang1, Xiang Yu Chen, Jian Sheng Li
1Department of Gastroenterology, the First Affiliated Hospital, Zhengzhou University, China.
Objective:
To determine the inhibitory effects of all-trans-retinoic acid (ATRA) on cell growth, cell cycle and vascular endothelial growth factor (VEGF) expression in the human gastric cancer cell line BGC-823 in vitro.
Methods:
Human gastric cancer BGC-823 cells were treated with various concentrations of ATRA and the cell growth was then determined using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide viability assay. The cell cycle distribution was analyzed using a flow cytometer. The VEGF mRNA and protein expression were analyzed by semi-quantitative RT-PCR and Western blotting, respectively.
Results:
ATRA at concentrations of 0.1-10 micromol/L inhibited the growth of BGC-823 cells grown in culture; a time- and dose-dependent inhibitory influence was found. ATRA arrested BGC-823 cells at the G0/G1 phase in a dose-dependent way. Both VEGF mRNA and protein were decreased by ATRA in a dose-dependent way.
Conclusion:
The anti-tumor effects of ATRA on human gastric cancer cells are associated with G0/G1 phase arrest and decreased VEGF expression.
Insights
All-trans-retinoic acid (ATRA) inhibits human gastric cancer cell growth by arresting cells in the G0/G1 phase and reducing vascular endothelial growth factor (VEGF) expression.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Gastric cancer remains a significant global health challenge.
- Understanding the molecular mechanisms of anti-cancer agents is crucial for developing effective therapies.
- All-trans-retinoic acid (ATRA) is a derivative of vitamin A with known biological activities.
Purpose of the Study:
- To investigate the in vitro effects of ATRA on human gastric cancer cell line BGC-823.
- To determine ATRA's impact on cell growth, cell cycle progression, and VEGF expression.
Main Methods:
- BGC-823 cells were treated with varying concentrations of ATRA.
- Cell viability was assessed using the MTT assay.
- Cell cycle distribution was analyzed via flow cytometry.
- VEGF mRNA and protein levels were quantified using RT-PCR and Western blotting, respectively.
Main Results:
- ATRA demonstrated a dose- and time-dependent inhibition of BGC-823 cell growth.
- ATRA induced a dose-dependent G0/G1 phase cell cycle arrest.
- Both VEGF mRNA and protein expression were significantly reduced by ATRA in a dose-dependent manner.
Conclusions:
- ATRA exhibits anti-tumor effects against human gastric cancer cells.
- These effects are mediated through G0/G1 phase arrest and downregulation of VEGF.
- ATRA represents a potential therapeutic agent for gastric cancer treatment.
