Noteborn M H
Leadd BV and Department of Molecular Cell Biology, Leiden University Medical Center, Wassenaarseweg 72, 2300 RA Leiden, The Netherlands.
Apoptosis. 1999 Oct;4(5):317-9. doi: 10.1023/a:1009687019221.
Apoptin, a protein encoded by an avian virus, induces apoptosis in various cultured human tumorigenic and/ or transformed cell lines, e.g. derived from breast and lung tumor, leukemia, lymphoma, osteosarcoma melanoma, cholangiocarcinoma, and hepatoma. In such cells, Apoptin induces p53-independent apoptosis, and the proto-oncogene Bcl-2 can accelerate this effect. The latter is surprising for, in general, Bcl-2 is known to inhibit e.g., p53-induced apoptosis. On the other hand, in normal non-transformed human cells, Apoptin is unable to induce apoptosis, even when Bcl-2 is over-expressed. In animal models Apoptin-induced apoptosis appears to be a safe and efficient anti-tumor agent. These data, in continuation with the observations that Apoptin is specifically stimulated by Bcl-2 in tumor cells, does not need p53, and is not inhibited by Bcr-Abl in these cells, imply that Apoptin is a potential anti-tumor therapy.
凋亡素是一种由禽病毒编码的蛋白质，可诱导多种培养的人类致瘤和/或转化细胞系发生凋亡，例如源自乳腺肿瘤、肺癌、白血病、淋巴瘤、骨肉瘤、黑色素瘤、胆管癌和肝癌的细胞系。在这类细胞中，凋亡素诱导不依赖p53的凋亡，原癌基因Bcl-2可加速这种效应。后者令人惊讶，因为一般而言，已知Bcl-2可抑制例如p53诱导的凋亡。另一方面，在正常未转化的人类细胞中，即使Bcl-2过表达，凋亡素也无法诱导凋亡。在动物模型中，凋亡素诱导的凋亡似乎是一种安全有效的抗肿瘤剂。这些数据，再加上凋亡素在肿瘤细胞中受到Bcl-2特异性刺激、不需要p53且不受这些细胞中Bcr-Abl抑制的观察结果，表明凋亡素是一种潜在的抗肿瘤疗法。
