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Published on: March 18, 2015
Arsenic trioxide induces apoptosis of human gastrointestinal cancer cells
Zhi-Bin Ma1, Hong-Yu Xu1, Miao Jiang1
1Zhi-Bin Ma, Hong-Yu Xu, Miao Jiang, You-Lin Yang, Lian-Xin Liu, Department of Gastroenterology, First Affiliated Hospital of Harbin Medical University, Harbin 150001, Heilongjiang Province, China.
Aim:
To investigate the changes in apoptosis in gastrointestinal cancer cells from patients with gastrointestinal cancers treated with arsenic trioxide (As₂O₃); and to study the possible molecular mechanisms of such changes by detecting the expression levels of p53 and Bcl-2.
Methods:
Twenty patients with gastrointestinal adenocarcinoma based on endoscopic and biopsy findings (ten patients with gastric cancer and ten patients with colorectal cancer) who received treatment in our hospital between August 2007 and December 2008 were included in this study. None of the patients had received anti-tumour agents prior to As₂O₃ treatment. As₂O₃ was administered intravenously at a dose of 0.01 g/d diluted with 5% glucose in normal saline for 2-3 h for 3 consecutive days before surgery. Morphological changes associated with apoptosis of gastrointestinal cancer cells were observed by light microscopy. Changes in the apoptotic index induced by As₂O₃ were investigated using the terminal deoxynucleotidyl transferase dUTP nick end labelling method. Expression levels of p53 and Bcl-2 proteins in gastrointestinal cancer tissues were determined by immunohistochemistry.
Results:
The apoptotic index of human gastrointestinal cancer cells was higher in cells from patients treated with As₂O₃ than in those not treated (P < 0.05). p53 protein expression in gastrointestinal tissues was unchanged by As₂O₃ (P > 0.05). However, Bcl-2 protein expression in gastrointestinal tissues was down-regulated by As₂O₃ (P < 0.01).
Conclusion:
These results demonstrate that As₂O₃ treatment in patients with gastrointestinal cancers can induce apoptosis in gastrointestinal cancer cells and down-regulate Bcl-2 protein expression.
Insights
Arsenic trioxide (As₂O₃) treatment increases apoptosis in gastrointestinal cancer cells. This study found As₂O₃ down-regulates Bcl-2 protein expression, suggesting a mechanism for its anti-cancer effects.
Area of Science:
- Oncology
- Molecular Biology
- Gastroenterology
Background:
- Gastrointestinal cancers pose a significant health burden globally.
- Arsenic trioxide (As₂O₃) is an established therapeutic agent with known anti-cancer properties.
- Understanding the molecular mechanisms of As₂O₃ in gastrointestinal cancers is crucial for optimizing treatment strategies.
Purpose of the Study:
- To investigate the effect of As₂O₃ on apoptosis in gastrointestinal cancer cells.
- To explore the role of p53 and Bcl-2 protein expression in mediating As₂O₃-induced apoptosis.
Main Methods:
- A cohort of 20 patients with gastrointestinal adenocarcinoma (gastric and colorectal) received As₂O₃ treatment prior to surgery.
- Apoptosis was assessed using morphological analysis and the terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) assay.
- Immunohistochemistry was employed to determine the expression levels of p53 and Bcl-2 proteins.
Main Results:
- As₂O₃ treatment significantly increased the apoptotic index in gastrointestinal cancer cells compared to untreated controls (P < 0.05).
- p53 protein expression remained unchanged following As₂O₃ treatment (P > 0.05).
- Bcl-2 protein expression was significantly down-regulated by As₂O₃ (P < 0.01).
Conclusions:
- Arsenic trioxide effectively induces apoptosis in gastrointestinal cancer cells.
- The down-regulation of Bcl-2 protein expression is a key molecular mechanism underlying As₂O₃'s apoptotic effects in these cancers.
