胃癌是最常见的肿瘤之一，目前胃癌的发生机制仍不十分清楚。microRNAs（miRNAs）作为一类新的癌基因或抑癌基因，参与各种癌症的发生和发展过程，包括胃癌。我们前期的研究证实，miR-25在人胃癌组织中高表达，采用Agomir系统使AGS细胞过表达miR-25,通过芯片筛选胃癌相关基因发现抗增殖蛋白Tob1/BTG2的表达显著下降，生物信息学预测发现miR-25种子序列靶向Tob1/BTG2的3'UTR，提示miR-25在AGS细胞中可能通过调节Tob1/BTG2发挥生物学功能。因此，我们的假设是：E2F1信号通路激活、启动子FoxO3上调或MCM7基因的甲基化水平降低导致miR-25的表达上调，抑制Tob1/BTG2的表达，进而通过Tob1/BTG2对细胞循环阻滞或PI3K/Akt、ErbB、TGF-β等信号通路中下游分子的影响,促进胃癌的发生。

Gastric cancer (GC) is one of the most common tumors, but the mechanism of gastric carcinogenesis remains unclear. MicroRNAs (miRNAs), which function as a novel class of oncogenes or tumor suppressor genes, participate in the occurrence of a variety of tumors, including GC. In previous study, we confirmed that miR-25 expression was increased in human gastric cancer tissue. MiR-25 was overexpressed in AGS cells by agomir system, and in these cells, we found the expression levels of Tob1/BTG2 were significantly decreased by mciroarray screening. Forthermore, we found that the seed sequence of miR-25 can target the 3' UTR of Tob1/BTG2 by bioinformatics analysis.These suggest that miR-25 may play a biological function by regulating Tob1/BTG2 expression in AGS cells. Therefore, our assumption is:miR-25 overexpression that may be caused by the excessive activity of E2F1 signaling pathway, FoxO3 upregulation or the declining methylation level of MCM7 gene inhibit Tob1/BTG2 expression, and then lead to cell cycle arrest or regulate the downstream effectors in PI3K/Akt, ErbB, TGF-βsignaling pathways, and, finally, trigger gastric carcinogenesis.