Jetten Anton M
Cell Biology Section, Immunity, Inflammation and Disease Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, 111 Alexander Drive, Research Triangle Park, NC 27709, USA.
Trends Cancer. 2019 Sep;5(9):547-557. doi: 10.1016/j.trecan.2019.07.005. Epub 2019 Aug 20.
GLI-similar 1-3 (GLIS1-3), a subfamily of Krüppel-like zinc finger transcription factors, function as key regulators of several biological processes important to oncogenesis, including control of cell proliferation, differentiation, self-renewal, and epithelial-mesenchymal transition. This review provides a short overview of the critical roles genetic changes in GLIS1-3 play in the development of several malignancies. This includes intrachromosomal translocations involving GLIS2 and ETO2/CBFA2T3 in the development of pediatric non-Down's syndrome (DS), acute megakaryoblastic leukemia (AMKL), a malignancy with poor prognosis, and an association of interchromosomal translocations between GLIS3, GLIS1, and PAX8, and between GLIS3 and CLPTM1L with hyalinizing trabecular tumors (HTTs) and fibrolamellar hepatocellular carcinoma (FHCC), respectively. Targeting upstream signaling pathways that regulate GLIS signaling may offer new therapeutic strategies in the management of cancer.
GLI 样 1 - 3（GLIS1 - 3）是一类 Kruppel 样锌指转录因子亚家族，作为对肿瘤发生至关重要的几个生物学过程的关键调节因子发挥作用，包括对细胞增殖、分化、自我更新和上皮 - 间质转化的控制。本综述简要概述了 GLIS1 - 3 基因变化在几种恶性肿瘤发生发展中所起的关键作用。这包括在小儿非唐氏综合征（DS）急性巨核细胞白血病（AMKL，一种预后不良的恶性肿瘤）发生过程中涉及 GLIS2 和 ETO2/CBFA2T3 的染色体内易位，以及分别在透明变性小梁肿瘤（HTT）和纤维板层肝细胞癌（FHCC）中 GLIS3 与 GLIS1、PAX8 之间以及 GLIS3 与 CLPTM1L 之间的染色体间易位。靶向调节 GLIS 信号传导的上游信号通路可能为癌症治疗提供新的策略。
