Abstract：
Gastric mucins serve as a protective barrier on the stomach\'s surface, protecting from external stimuli including gastric acid and gut microbiota. Their composition typically changes in response to the metaplastic sequence triggered by Helicobacter pylori infection. This alteration in gastric mucins is also observed in cases of gastric cancer, although the precise connection between mucin expressions and gastric carcinogenesis remains uncertain. This review first introduces the relationship between mucin expressions and gastric metaplasia or cancer observed in humans and mice. Additionally, we discuss potential pathogenic mechanisms of how aberrant mucins and their glycans affect gastric carcinogenesis. Finally, we summarize challenges to target tumor-specific glycans by utilizing lectin-drug conjugates that can bind to specific glycans. Understanding the correlation and mechanism between these mucin expressions and gastric carcinogenesis could pave the way for new strategies in gastric cancer treatment.
摘要：
胃粘蛋白作为胃表面的保护屏障，保护免受外部刺激，包括胃酸和肠道微生物群。它们的组成通常响应于由幽门螺杆菌感染引发的化生序列而改变。在胃癌病例中也观察到胃粘蛋白的这种改变，尽管粘蛋白表达与胃癌发生之间的确切联系仍不确定。这篇综述首先介绍了在人类和小鼠中观察到的粘蛋白表达与胃上皮化生或癌症之间的关系。此外,我们讨论了异常粘蛋白及其聚糖如何影响胃癌发生的潜在致病机制。最后,我们总结了利用可与特定聚糖结合的凝集素-药物偶联物靶向肿瘤特异性聚糖的挑战.了解这些粘蛋白表达与胃癌发生之间的相关性和机制，可以为胃癌治疗的新策略铺平道路。
