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Selenium and sulindac are synergistic to inhibit intestinal tumorigenesis in Apc/p21 mice
Xiuli Bi1, Nicole Pohl, Huali Dong
1School of Life Sciences, Liaoning University, Shenyang 110036, China.
Background:
Both selenium and non-steroidal anti-inflammatory drug (NSAID) sulindac are effective in cancer prevention, but their effects are affected by several factors including epigenetic alterations and gene expression. The current study was designed to determine the effects of the combination of selenium and sulindac on tumor inhibition and the underlying mechanisms.
Results:
We fed the intestinal tumor model Apc/p21 mice with selenium- and sulindac-supplemented diet for 24 weeks, and found that the combination of selenium and sulindac significantly inhibited intestinal tumorigenesis, in terms of reducing tumor incidence by 52% and tumor multiplicities by 80% (p<0.01). Mechanistic studies revealed that the combination of selenium and sulindac led to the significant induction of the expression of p27 and p53 and JNK1 phosphorylation, and led to the suppression of β-catenin and its downstream targets. Impressively, the data also showed that demythelation on p21 promoter was associated with tumor inhibition by the combination of selenium and sulindac.
Conclusions:
The selenium is synergistic with sulindac to exert maximal effects on tumor inhibition. This finding provides an important chemopreventive strategy using combination of anti-cancer agents, which has a great impact on cancer prevention and has a promising translational potential.
Insights
Combining selenium and non-steroidal anti-inflammatory drug (NSAID) sulindac significantly inhibits intestinal tumors. This synergistic approach offers a promising chemopreventive strategy with broad cancer prevention potential.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Prevention
Background:
- Selenium and NSAID sulindac show cancer chemopreventive potential.
- Epigenetic alterations and gene expression influence their efficacy.
- Understanding combined effects is crucial for optimizing cancer prevention strategies.
Purpose of the Study:
- To investigate the combined effects of selenium and sulindac on tumor inhibition.
- To elucidate the underlying molecular mechanisms of their synergistic action.
Main Methods:
- Apc/p21 mice, an intestinal tumor model, were fed a diet supplemented with selenium and sulindac for 24 weeks.
- Tumor incidence and multiplicity were assessed.
- Mechanistic studies involved analyzing gene expression (p27, p53, β-catenin), JNK1 phosphorylation, and promoter methylation (p21).
Main Results:
- The combination significantly reduced intestinal tumor incidence by 52% and tumor multiplicities by 80% (p<0.01).
- Key molecular changes included induced expression of p27 and p53, increased JNK1 phosphorylation, and suppressed β-catenin signaling.
- Tumor inhibition correlated with demethylation of the p21 promoter.
Conclusions:
- Selenium and sulindac exhibit synergistic effects for maximal tumor inhibition.
- This combination represents a potent chemopreventive strategy with significant translational potential for cancer prevention.
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