Abstract
Background: Colonic mucinous adenocarcinoma is a highly aggressive subtype of colon cancer. Epidemiological evidence has linked estrogen exposure to certain gastrointestinal malignancies, yet its pathophysiological role in the pathogenesis of colonic mucinous adenocarcinoma remains unclear. This study aimed to investigate the effect of estrogen on tumor growth in a rat model of colonic mucinous adenocarcinoma and its association with intestinal mucosal epithelial proliferation-related factors and apoptosis.
Results: Compared with the normal control group, the model control group showed significantly increased tumor proliferative activity and elevated intestinal epithelial apoptosis. After estrogen intervention, tumor volume and proliferative activity were inhibited, the expressions of Ki-67 and proliferating cell nuclear antigen were downregulated, and the apoptosis rate of intestinal epithelial cells decreased; an estrogen antagonist could enhance some of the above effects.
Conclusions: Estrogen can slow the growth of colonic mucinous adenocarcinoma by inhibiting intestinal mucosal epithelial proliferation, exhibiting potential anti-tumor effects. Its mechanism may be related to regulating the proliferation-apoptosis balance of intestinal mucosal epithelium, providing experimental evidence for colon cancer therapy research.
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