Wang Rui, Hu Yi, Song Ge, Hao Chan Juan, Cui Yi, Xia Hong-Fei, Ma Xu
Reproductive and Genetic Center of National Research Institute for Family Planning, Beijing, China.
Cell Physiol Biochem. 2012;29(3-4):381-90. doi: 10.1159/000338493. Epub 2012 Apr 3.
MiR-206 was involved in a series of cellular activities, such as the growth and development of skeletal muscle and the tumorigenesis. MiR-206 was characterized previously as a differentially expressed gene in sodium arsenite (SA)-induced neural tube defects (NTDs) in chick embryos via miRNA microarray analysis. However, the role of miR-206 in the pathological process of nerve cells remained elusive. In this study we found differential expression of miR-206 in SA-treated chick embryos by Northern blot analysis. Ectopic expression of miR-206 inhibited cell proliferation, and promoted cell apoptosis in U343 and SK-N-SH cell by using MTT, Edu Apollo assay and Flow cytometry analysis. Further investigation revealed that miR-206 can interact with 3'-untranslated region (UTR) of Otx2. MiR-206 mimics down-regulated the endogeneous Otx2 expression, whereas the miR-206 inhibitor obviously up-regulated the expression of Otx2. These findings indicate that overexpression of miR-206 promotes cell apoptosis and low expression of miR-206 inhibits cell apoptosis. Otx2 may play an important role in the process of miR-206-mediated cell apoptosis.
微小RNA-206（MiR-206）参与了一系列细胞活动，如骨骼肌的生长发育以及肿瘤发生。先前通过微小RNA微阵列分析，MiR-206被鉴定为在亚砷酸钠（SA）诱导的鸡胚神经管缺陷（NTDs）中差异表达的基因。然而，MiR-206在神经细胞病理过程中的作用仍不清楚。在本研究中，我们通过Northern印迹分析发现在SA处理的鸡胚中MiR-206表达存在差异。通过MTT、Edu Apollo检测法和流式细胞术分析，MiR-206的异位表达抑制了U343和SK-N-SH细胞的增殖并促进了细胞凋亡。进一步研究表明，MiR-206可与Otx2的3'-非翻译区（UTR）相互作用。MiR-206模拟物下调了内源性Otx2的表达，而MiR-206抑制剂则明显上调了Otx2的表达。这些发现表明，MiR-206的过表达促进细胞凋亡，而MiR-206的低表达抑制细胞凋亡。Otx2可能在MiR-206介导的细胞凋亡过程中起重要作用。
