Department of Otolaryngology, Head and Neck Surgery, The First Hospital, Shanxi Medical University, Taiyuan, Shanxi, China.
FEBS Lett. 2013 Oct 1;587(19):3166-74. doi: 10.1016/j.febslet.2013.05.069. Epub 2013 Aug 1.
Our study focuses on a set of laryngeal tumors that show reduced RUNX3 expression in the absence of transcriptional silencing of tumor suppressor gene RUNX3 by aberrant methylation of CpG islands. We report that the loss of expression of RUNX3 correlates with up-regulation of miR-106b in human laryngeal carcinoma tissue. The downregulation of RUNX3 is mediated by miR-106b through binding of its 3'UTR. Moreover, miR-106b can promote the proliferation and invasion of laryngeal carcinoma cells by directly targeting RUNX3, and RUXN3 knockdown can abolish this phenotype. These results shed a new insight into the mechanism of miRNA regulation in laryngeal carcinoma.
我们的研究集中在一组喉肿瘤上,这些肿瘤在没有 RUNX3 肿瘤抑制基因因 CpG 岛异常甲基化而转录沉默的情况下,表现出 RUNX3 表达降低。我们报告说,RUNX3 的表达缺失与人喉癌组织中 miR-106b 的上调相关。RUNX3 的下调是由 miR-106b 通过结合其 3'UTR 介导的。此外,miR-106b 可以通过直接靶向 RUNX3 促进喉癌细胞的增殖和侵袭,而 RUNX3 的敲低可以消除这种表型。这些结果为 miRNA 调节喉癌的机制提供了新的见解。