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Published on: March 18, 2015
Arsenic trioxide regulates gastric cancer cell apoptosis by mediating cAMP
A Abudoureyimu1, A Muhemaitibake
1Department of Geriatrics, Xinjiang Medical University Affiliated Hospital of Traditional Chinese Medicine, Urumqi, Xinjiang, China. HongyuZhengzxc@163.com.
Objective:
Gastric cancer is a common digestive tract tumor in clinic with increasing incidence. It is suggested that arsenic trioxide (As2O3) has an inhibitory effect on many kinds of digestive system tumors. This study evaluated the impact of As2O3 on the apoptosis of gastric cancer BGC-823 cells, and analyzed its relationship with cyclic adenosine monophosphate (cAMP).
Materials And Methods:
Gastric cancer cell BGC-823 was intervened by different concentrations of As2O3 at 4 ng/ml, 8 ng/ml, and 16 ng/ml, respectively. BGC-823 cell apoptosis was evaluated by TUNEL assay. Cell cycle was determined by flow cytometry. cAMP and protein kinase C (PKC) was detected by radioimmunoassay. Apoptosis-related protein levels were tested by Western blot.
Results:
Compared with normal control, As2O3 significantly increased BGC-823 cell apoptosis, blocked cell cycle in G0/G1 phase, elevated cAMP and Bax level, as well as downregulated PKC, Bcl-2 and Survivin expression (p < 0.05).
Conclusions:
As2O3 induced BGC-823 cell apoptosis through the up-regulation of the cAMP level and the decrease of the PKC level.
Insights
Arsenic trioxide (As2O3) promotes apoptosis in gastric cancer cells by increasing cyclic adenosine monophosphate (cAMP) and decreasing protein kinase C (PKC). This study investigates As2O3
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Gastric cancer is a prevalent malignancy with rising incidence.
- Arsenic trioxide (As2O3) shows promise in inhibiting digestive system tumors.
Purpose of the Study:
- To investigate the effect of As2O3 on gastric cancer BGC-823 cell apoptosis.
- To analyze the relationship between As2O3, apoptosis, cyclic adenosine monophosphate (cAMP), and protein kinase C (PKC).
Main Methods:
- Gastric cancer BGC-823 cells were treated with varying concentrations of As2O3.
- Apoptosis was assessed using TUNEL assay.
- Cell cycle, cAMP, PKC, and apoptosis-related proteins were analyzed via flow cytometry, radioimmunoassay, and Western blot.
Main Results:
- As2O3 significantly increased BGC-823 cell apoptosis.
- Cell cycle arrest was observed in the G0/G1 phase.
- cAMP and Bax levels increased, while PKC, Bcl-2, and Survivin expression decreased.
Conclusions:
- As2O3 induces apoptosis in gastric cancer cells.
- The mechanism involves up-regulation of cAMP and down-regulation of PKC.
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