Battista S, de Nigris F, Fedele M, Chiappetta G, Scala S, Vallone D, Pierantoni G M, Mega T, Santoro M, Viglietto G, Verde P, Fusco A
Instituto Nazionale dei Tumori di Napoli, Fondazione Senatore Pascale, Oncologia Sperimentale D ed E, Italia.
Oncogene. 1998 Jul 23;17(3):377-85. doi: 10.1038/sj.onc.1201953.
We have recently reported that neoplastic transformation of two rat thyroid epithelial cell lines by retroviruses carrying the v-mos and v-ras Ki oncogenes is associated with a drastic increase of AP-1 activity. The most important effects were represented by the dramatic junB and fra-1 gene induction, which was abolished by the block of the transformation-induced HMGI-C protein synthesis. Here, we have further characterized the transformation-dependent AP-1 activity, by analysing the expression of different jun- and fos-related components, in rat thyroid cell lines transformed by several oncogenes, in human thyroid carcinoma cell lines, and in naturally occurring human thyroid tumours. A significant increase of Fra-1 and JunB protein levels was detected in all oncogene transformed rat thyroid cell lines. Fra-1 gene induction was demonstrated to occur also in human thyroid carcinoma cell lines and tissues. Conversely, c-Jun and JunD proteins, rather than JunB, accumulated in human thyroid carcinoma cell lines. An induction of AP-1 target genes was also detected both in rat and human thyroid transformed cell lines. Therefore, in vivo and in vitro thyroid cell transformation is associated with important compositional changes in the AP-1 complex and an increased transcriptional activity.
我们最近报道,携带v-mos和v-ras Ki癌基因的逆转录病毒对两种大鼠甲状腺上皮细胞系进行肿瘤转化与AP-1活性的急剧增加有关。最重要的影响表现为junB和fra-1基因的显著诱导,而这种诱导在转化诱导的HMGI-C蛋白合成受阻时被消除。在此,我们通过分析几种癌基因转化的大鼠甲状腺细胞系、人甲状腺癌细胞系以及自然发生的人甲状腺肿瘤中不同jun和fos相关成分的表达,进一步对依赖转化的AP-1活性进行了表征。在所有癌基因转化的大鼠甲状腺细胞系中均检测到Fra-1和JunB蛋白水平显著增加。Fra-1基因的诱导在人甲状腺癌细胞系和组织中也被证实会发生。相反,在人甲状腺癌细胞系中积累的是c-Jun和JunD蛋白,而非JunB。在大鼠和人甲状腺转化细胞系中均检测到AP-1靶基因的诱导。因此,体内和体外甲状腺细胞转化与AP-1复合物的重要组成变化以及转录活性增加有关。