人肿瘤中Myc诱导的p53依赖性细胞凋亡的失活。

Inactivation of Myc-induced p53-dependent apoptosis in human tumors.

作者信息

Henriksson M, Selivanova G, Lindström M, Wiman K G

机构信息

Microbiology and Tumor Biology Center, Karolinska Institutet, Stockholm, Sweden.

出版信息

Apoptosis. 2001 Feb-Apr;6(1-2):133-7. doi: 10.1023/a:1009644716727.

DOI:10.1023/a:1009644716727

PMID:11321036

Abstract

The Myc family of oncoproteins promote cell growth and are frequently overexpressed in human tumors. However, Myc can also trigger cell death by apoptosis. This is at least in part mediated via the ARF-p53 pathway. Myc activation leads to a selection for inactivation of ARF or p53, allowing cell survival and tumor progression. Restoration of p53-dependent apoptosis by various means is an attractive approach for new cancer therapy.

摘要

致癌蛋白Myc家族促进细胞生长，且在人类肿瘤中常常过度表达。然而，Myc也可通过凋亡触发细胞死亡。这至少部分是通过ARF-p53途径介导的。Myc激活导致对ARF或p53失活的选择，从而使细胞存活和肿瘤进展。通过各种手段恢复p53依赖性凋亡是一种有吸引力的新型癌症治疗方法。