蜗牛蛋白调控腭部发生发育的机制
Mechanisms of the transcript factor Snail during palatogenesis

摘要： 蜗牛蛋白（Snail）参与调控腭部融合过程中腭中缝上皮（MES）细胞的上皮间质转化（EMT）、程序性细胞死亡（PCD）或存活以及细胞迁移等生物学行为，Snail基因失去了转化生长因子-β3的抑制而表达水平升高，此时Snail作为MEE/MES细胞的存活因子，导致腭中线上皮（MEE）/MES细胞持续存在并诱发腭裂。Snail基因编码具有锌指结构的Snail1、Snail2和Snail3等转录因子，其家族具有相似的结构，可以结合到E-钙黏蛋白的启动子，抑制其表达，可以在胚胎发生发育和肿瘤转移过程中诱导EMT。Snail基因可防止细胞因为存活因子的减少或PCD因子的积累而死亡，故Snail基因是MEE/MES细胞的存活因子和细胞运动的诱导因子。微小RNA（miRNA）不仅在人类癌细胞中发挥着重要的作用，而且在胚胎健康发育过程中必不可少。miRNA表达模式的变异和miRNA在mRNA的结合位点的结构变异，可能导致颅面发育变异。本文就Snail基因结构与功能、Snail基因在侧腭突发育过程中表达、Snail基因与MEE/MES细胞的EMT、Snail基因与MEE/MES程序性细胞死、Snail基因是MEE/MES细胞的存活因子、微小RNA调控Snail在MEE/MES消失过程中的作用等研究进展作一综述。
Abstract: Snail is involved in epithelial-to-mesenchymal transformation(EMT), programmed cell death(PCD), and medial epithelial seam(MES) cell migration during palatogenesis. The Snail expression becomes upregulated without inhibiting transforming growth factor(TGF)-β3 and causes cleft palate. Snail gene-encoding transcript factors, namely, Snail1, Snail2, and Snail3, can combine with the promoter of E-cadherin and inhibit its expression; these factors then induce EMT during embryogenesis and tumor metastasis. Snail is also a critical factor of MEE/MES cell survival and cell migration. MicroRNA(miRNA) are another important factor in embryogenesis. Variation in the expression pattern and mRNA binding sites of miRNA can lead to craniofacial anomalies. This review introduces the structure, functions, and expression of Snail during palatogenesis. This review also discusses the relation of Snail to EMT, PCD, and cell survival during the disappearance of MEE/MES. This review also describes the mechanisms by which miRNA regulate Snail to control the disappearance of MEE/MES