Lodygin Dmitri, Hermeking Heiko
Molecular Oncology, Independent Max-Planck Research Group, Max-Planck-Institute of Biochemistry, Martinsried, Munich, Germany.
Semin Cancer Biol. 2006 Jun;16(3):214-24. doi: 10.1016/j.semcancer.2006.03.008. Epub 2006 Apr 1.
The 14-3-3sigma gene is a direct target of the p53 tumor suppressor and its product inhibits cell cycle progression. Recently, a proteomic analysis revealed that 14-3-3sigma regulates additional cellular processes relevant to carcinogenesis, as migration and MAP-kinase signalling. The expression of 14-3-3sigma is down-regulated by CpG methylation in several types of human cancer, among them prostate, lung, breast and several types of skin cancer. The epigenetic inactivation of 14-3-3sigma occurs at an early stage of tumor development and may allow evasion from senescence and promote genomic instability. In the future the detection of CpG methylation of 14-3-3sigma may be used for diagnostic and prognostic purposes.
14-3-3σ基因是p53肿瘤抑制因子的直接靶点，其产物可抑制细胞周期进程。最近，一项蛋白质组学分析表明，14-3-3σ还调控与癌症发生相关的其他细胞过程，如迁移和丝裂原活化蛋白激酶信号传导。在几种人类癌症中，包括前列腺癌、肺癌、乳腺癌和几种皮肤癌，14-3-3σ的表达因CpG甲基化而下调。14-3-3σ的表观遗传失活发生在肿瘤发展的早期阶段，可能导致细胞逃避衰老并促进基因组不稳定。未来，检测14-3-3σ的CpG甲基化可用于诊断和预后评估。
