沉默FOXQ1可逆转SW480细胞的上皮-间质转化

FOXQ1是FOX家族的的重要成员之一，其参与了多种人类肿瘤的上皮间质转化(epithelial- mesenchymal transition，EMT).本研究设计合成了FOXQ1基因的shRNA（short hairpin RNA），用此转染SW480细胞，通过显微镜观察细胞形态，Transwell小室、细胞黏附试验检测转移能力及黏附能力,以探索FOXQ1与结直肠癌细胞EMT的关系.结果显示,沉默FOXQ1后，SW480细胞顶底极性及细胞间紧密连接增加，侵袭、迁移的细胞数目减少，同种黏附能力增加,异种黏附能力降低.进一步的机制研究表明,沉默FOXQ1基因可以导致SW480细胞的上皮标志因子E-cadherin表达显著增高,而间质细胞标志因子N-cadherin、Vimentin及MMP2表达均降低.以上结果表明，沉默FOXQ1基因可以逆转SW480细胞EMT，其机制可能与E-cadherin的上调和N cadherin、Vimentin、MMP2的下调有关，这为进一步研究FOXQ1在结直肠癌发生发展中的作用提供实验基础.

Silencing FOXQ1 Counteracts EMT in Human Colorectal Cancer SW480 Cells

FOXQ1 is a member of the FOX family, and is discovered to participate in human tumor epithelial-mesenchymal transition (EMT). To explore the effect of FOXQ1 in colorectal cancer cells, short-hairpin RNA (shRNA) of FOXQ1 was introduced into SW480 cells. Cell metastasis, adhesion and migration were investigated by transwell and adhesion experiments. Cell morphology was examined under the microscope. The results showed that after FOXQ1 silencing changed SW480 cells polarity and increased tight junctions. Cell invasion and migration abilities were reduced, homogeneous cell adhesion was increased and heterogeneous adhesion was decreased. The expression of epithelial marker gene E-cadherin was significantly upregulated| mesenchymal marker genes of N-cadherin, vimentin and MMP-2 were downregulated. These findings suggested that silencing of FOXQ1 might inhibit metastasis by attenuating EMT in colorectal cancer SW480 cells. The importance of FOXQ1 in colorectal cancer development deserves further investigation．