Burtscher I, Compagni A, Lamm G M, Christofori G
Research Institute of Molecular Pathology, Vienna, Austria.
Cancer Res. 1999 Aug 15;59(16):3923-6.
Hyperproliferation of tumor cells usually coincides with increased tumor cell apoptosis. To overcome apoptosis, tumor cells frequently induce the expression of growth factors that mediate cell survival. In nontransformed cells, including fibroblasts and neurons, survival factor-mediated signal transduction involves the activation of phosphatidylinositol 3' kinase (PI-3K) and protein kinase B/c-Akt (PKB). Here we demonstrate that tumor cell lines derived from a transgenic mouse model of pancreatic beta cell carcinogenesis use insulin-like growth factors to repress apoptosis independently of PI-3K and PKB. The results indicate that tumor cells can use additional survival signal transduction pathways.
肿瘤细胞的过度增殖通常与肿瘤细胞凋亡增加同时发生。为了克服凋亡，肿瘤细胞经常诱导介导细胞存活的生长因子的表达。在包括成纤维细胞和神经元在内的未转化细胞中，存活因子介导的信号转导涉及磷脂酰肌醇3'激酶（PI-3K）和蛋白激酶B/c-Akt（PKB）的激活。在此，我们证明，源自胰腺β细胞癌变转基因小鼠模型的肿瘤细胞系利用胰岛素样生长因子独立于PI-3K和PKB来抑制凋亡。结果表明，肿瘤细胞可以利用其他存活信号转导途径。
