Lanzi C, Borrello M G, Bongarzone I, Migliazza A, Fusco A, Grieco M, Santoro M, Gambetta R A, Zunino F, Della Porta G
Divisione di Oncologia Sperimentale B, Istituto Nazionale Tumori, Milan, Italy.
Oncogene. 1992 Nov;7(11):2189-94.
In papillary thyroid carcinomas, we have identified two tumor-specific rearrangements of the RET proto-oncogene leading to the formation of different transforming fusion products sharing the tyrosine kinase (tk) domain of the proto-oncogene and designated ptc-1 and ptc-2. We have analysed ptc-1 and ptc-2 products by immunoprecipitation with specific anti-RET antibodies followed by immunoblotting with the same reagent or with antibodies specific for phosphotyrosine (P-tyr) residues. The anti-RET antibodies were reactive with 64-kDa (p64ptc-1) and 81-kDa (p81ptc-2) proteins from lysates of ptc-1 and ptc-2 transformed cells, respectively, and identified two proteins of 140 kDa and 160 kDa from extracts of SK-N-SH, a neuroblastoma cell line previously shown to express two differently glycosylated forms of the normal RET product. The anti P-tyr antibodies, while detecting the same p64ptc-1 and p81ptc-2 proteins from ptc-1 and ptc-2 extracts, did not show any specific band in the neuroblastoma lysates. An additional set of experiments led us to conclude that, whereas the normal product of the RET proto-oncogene is a membrane-associated receptor-like molecule not intrinsically phosphorylated on tyrosine, both oncogenic forms of RET, ptc-1 and ptc-2, are constitutively phosphorylated on tyrosine, display an 'in vitro' autophosphorylation activity, are translocated from the membrane to the cytoplasm and are apparently unaffected by protein kinase C modulation.
在甲状腺乳头状癌中,我们鉴定出RET原癌基因的两种肿瘤特异性重排,导致形成不同的转化融合产物,这些产物共享原癌基因的酪氨酸激酶(tk)结构域,分别命名为ptc-1和ptc-2。我们通过用特异性抗RET抗体进行免疫沉淀,然后用相同试剂或针对磷酸酪氨酸(P-tyr)残基的抗体进行免疫印迹,分析了ptc-1和ptc-2产物。抗RET抗体分别与来自ptc-1和ptc-2转化细胞裂解物的64 kDa(p64ptc-1)和81 kDa(p81ptc-2)蛋白发生反应,并从SK-N-SH(一种先前显示表达正常RET产物的两种不同糖基化形式的神经母细胞瘤细胞系)提取物中鉴定出140 kDa和160 kDa的两种蛋白。抗P-tyr抗体在检测来自ptc-1和ptc-2提取物的相同p64ptc-1和p81ptc-2蛋白时,在神经母细胞瘤裂解物中未显示任何特异性条带。另一组实验使我们得出结论,RET原癌基因的正常产物是一种膜相关的受体样分子,其酪氨酸本身不被磷酸化,而RET的两种致癌形式ptc-1和ptc-2在酪氨酸上组成性磷酸化,具有“体外”自磷酸化活性,从膜转移到细胞质,并且显然不受蛋白激酶C调节的影响。