Department of Dermatology and Skin Science, Jack Bell Research Centre, Vancouver Coastal Health Research Institute, University of British Columbia, 2660 Oak Street, Vancouver, BC, V6H 3Z6, Canada.
Cell Mol Life Sci. 2010 Jun;67(12):1987-99. doi: 10.1007/s00018-010-0312-z. Epub 2010 Mar 2.
The inhibitor of growth (ING) family of tumor suppressors has five members and is implicated in the control of apoptosis, senescence, DNA repair, and cancer progression. However, little is known about ING activity in the regulation of cancer progression. ING members and splice variants seem to behave differently with respect to cancer invasion and metastasis. Interaction with histone trimethylated at lysine 4 (H3K4me3), hypoxia inducible factor-1 (HIF-1), p53, and nuclear factor kappa-B (NF-kappaB) are potential mechanisms by which ING members exert effects on invasion and metastasis. Subcellular mislocalization, rapid protein degradation, and to a lesser extent ING gene mutation are among the mechanisms responsible for inappropriate ING levels in cancer cells. The aim of this review is to summarize the different roles of ING family tumor suppressors in cancer progression and the molecular mechanisms involved.
抑生长因子(ING)家族的肿瘤抑制因子有五个成员,参与细胞凋亡、衰老、DNA 修复和癌症进展的调控。然而,ING 在癌症进展中的作用知之甚少。ING 成员和剪接变异体在癌症侵袭和转移方面的表现似乎有所不同。ING 成员与组蛋白赖氨酸 4 三甲基化(H3K4me3)、缺氧诱导因子-1(HIF-1)、p53 和核因子 kappa-B(NF-kappaB)的相互作用是 ING 成员发挥侵袭和转移作用的潜在机制。亚细胞定位错误、蛋白质快速降解以及在较小程度上 ING 基因突变是导致癌细胞中 ING 水平异常的机制。本文综述了 ING 家族肿瘤抑制因子在癌症进展中的不同作用及其相关的分子机制。