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胃泌素(Gastrin)和胆囊收缩素(CCK)对消化道上皮的生长营养作用20多年来一直激励着人们对其与消化道肿瘤关系的不懈探索,但除起源于ECL(Enterchromaffin-like)细胞的胃类癌外,胃肠G/I细胞分泌的成熟酰胺化Gastrin/CCK(G-NH_2/CCK-NH_2)与消化道肿瘤发生的关系尚不明确。近年研究表明,在消化道上皮细胞转化过程中,自身的Gastrin/CCK基因也异常激活,同时其翻译后加工能力又受到不同程度的损害,常经固有性途径分泌大量Gastrin/CCK原(Pro G/Pro CCK)及甘氨酸延伸型中间产物(G-gly/CCK-gy),与其自身的相应受体形成自分
The nutritional effects of gastrin and cholecystokinin (CCK) on the epithelium of the gastrointestinal tract have been stimulating for more than two decades for their association with gastrointestinal tumors. However, in addition to the cells derived from the cells of ECL (Enterchromaffin-like) (G-NH2 / CCK-NH2) secreted by gastrointestinal G / I cells and gastrointestinal carcinogenesis is unclear. Recent studies show that Gastrin / CCK gene is also abnormally activated in the process of gastrointestinal epithelial cell transformation, and its posttranslational processing ability is impaired to different extents, often secreting large amounts of Gastrin / CCK (Pro G / Pro CCK) and glycine extended intermediate (G-gly / CCK-gy), forming their own