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首页> 外文期刊>Cell biology international. >TYRPHOSTIN INDUCES NON-APOPTOTIC PROGRAMMED CELL DEATH IN COLON TUMOR CELLS
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TYRPHOSTIN INDUCES NON-APOPTOTIC PROGRAMMED CELL DEATH IN COLON TUMOR CELLS

机译：酪蛋白诱导结肠癌细胞中非凋亡的程序性细胞死亡

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摘要

The programmed cell death inducing effect of the EGF receptor tyrosine kinase inhibitor alpha-cyano-3,4-dihydroxycinnamthioamide (AG213) was investigated in vitro on HT-29 human colon tumor. AG213 at concentrations between 45 to 450 mu M blocks the proliferation of HT-29 cells. Morphological findings suggest that the selective tyrosine kinase inhibitor AG213 induces Clarke III type (non-lysosomal vesiculate cytoplasmic) programmed cell death; unlike ATP analog nonselective tyrosine kinase inhibitors like Genistein which were found to induce apoptosis. Cycloheximide and Actinomycin-D reduced the effect of AG213 pointing to the fact that protein and RNA synthesis are also needed for this form of cell death. Acid phosphatase activity was found in the Golgi and in the newly formed intracytoplasmic vacuoles 3 hours after AG213 treatment which disappeared by 6 hours. The induction of Clarke III cell death by tyrosine kinase inhibitors may open a new modality to selective killing of tumor cells.
机译：在体外研究了EGF受体酪氨酸激酶抑制剂α-氰基-3,4-二羟基肉桂硫代酰胺（AG213）对HT-29人结肠肿瘤的程序性细胞死亡诱导作用。浓度在45至450μM之间的AG213阻断了HT-29细胞的增殖。形态学发现表明，选择性酪氨酸激酶抑制剂AG213诱导Clarke III型（非溶酶体囊泡细胞质）程序性细胞死亡。与ATP类似物非选择性酪氨酸激酶抑制剂（如Genistein）不同，后者可诱导细胞凋亡。环己酰亚胺和放线菌素D降低了AG213的作用，表明这种形式的细胞死亡也需要蛋白质和RNA合成。在AG213处理3小时后，在高尔基体和新形成的胞质内液泡中发现了酸性磷酸酶活性，在6小时后消失。酪氨酸激酶抑制剂诱导Clarke III细胞死亡可能为选择性杀死肿瘤细胞打开新的模式。

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