TUMOR PROMOTER INDUCED PROTEIN PHOSPHORYLATION

人结肠上皮细胞的转化赋予它们 对新的促有丝分裂信号的敏感性。 粪便甘油二酯（DG），组成 油酸，肉豆蔻酸，或棕榈酸残基，在体内发现在uM， mM浓度（Cancer Res.49：544-548，1989），并且可能源自 从膳食脂肪中。 当DG加入体外培养的结肠细胞中时， 洗涤剂胶束在生理浓度，他们诱导 癌前结肠细胞、某些癌细胞增殖，但不 正常结肠细胞（同上）。 DGs也增加尿激酶分泌， 癌细胞 与这种对肿瘤的选择性生物活性平行的是， 细胞，粪便甘油二酯诱导酪氨酸残基的磷酸化 在癌和腺瘤细胞中有一个63 kd的膜蛋白，但在正常细胞中没有 细胞，如用抗磷酸酪氨酸单克隆抗体免疫印迹所示 抗体的 我们建议继续研究信号的机制 DG通过酪氨酸激酶在结肠细胞中启动的转导 底物pp 63。

Transformation of human colonic epithelial cells confers on them sensitivity to new mitogenic signals. Fecal diglycerides (DGs), composed of oleic, myristic, or palmitic acid residues, were found in vivo at uM to mM concentrations (Cancer Res.49 :544-548, 1989), and were probably derived from dietary fat. When DGs were added to colon cells in vitro in detergent-micelles at physiological concentrations, they induced proliferation of premalignant colonocytes, some carcinoma cells, but not normal colonocytes (ibid). DGs also increased urokinase secretion from carcinoma cells. Parallel to this selective biological activity on tumor cells, fecal diglycerides induced the phosphorylation on tyrosine residues of a 63 kd membrane protein in carcinoma and adenoma cells but not normal cells, as shown by immunoblotting with antiphosphotyrosine monoclonal antibody. We propose to continue to study the mechanism of signal transduction initiated by DGs in colon cells through the tyrosine kinase substrate pp63.