Department of Colorectal Surgery, Shaoxing People's Hospital, Shaoxing Hospital of Zhejiang University, Shaoxing, 312000, Zhejiang, China.
Dig Dis Sci. 2014 Sep;59(9):2145-52. doi: 10.1007/s10620-014-3159-6. Epub 2014 Apr 19.
We hypothesized that miR-194 may control Forkhead box protein M1 (FoxM1) expression in gastric cancer cells and therefore may have therapeutic potential in gastric cancer.
The expression level of miR-194 was examined using real-time PCR in human gastric cancer and noncancerous gastric tissues, gastric cancer cell and normal gastric mucosal epithelial cell. We examined whether the miR-194 regulates cell migration and invasion, and the epithelial-mesenchymal transition Phenotype by inhibiting FoxM1 in gastric cancer cells.
The expression of miR-194 was significantly lower in gastric cancer compared with non-cancerous gastric tissues and cells. Exogenous expression of miR-194 inhibited cell migration, invasion, and the epithelial-mesenchymal transition phenotype in gastric cancer cells. Moreover, we discovered a novel post-transcriptional regulatory mechanism of FoxM1 expression that is mediated by miR-194.
Our study clearly demonstrates that miR-194 inhibits the acquisition of the EMT phenotype in gastric cancer cells by downregulating FoxM1, thereby inhibiting cell migration and invasion during cancer progression.
我们假设 miR-194 可能控制胃癌细胞中的叉头框蛋白 M1(FoxM1)表达,因此在胃癌中可能具有治疗潜力。
使用实时 PCR 检测人胃癌和非癌性胃组织、胃癌细胞和正常胃黏膜上皮细胞中 miR-194 的表达水平。我们通过抑制胃癌细胞中的 FoxM1 来检测 miR-194 是否调节细胞迁移和侵袭以及上皮-间充质转化表型。
与非癌性胃组织和细胞相比,胃癌中 miR-194 的表达明显降低。外源性表达 miR-194 抑制了胃癌细胞的迁移、侵袭和上皮-间充质转化表型。此外,我们发现了一种由 miR-194 介导的 FoxM1 表达的新型转录后调控机制。
我们的研究清楚地表明,miR-194 通过下调 FoxM1 抑制胃癌细胞中 EMT 表型的获得,从而抑制癌症进展过程中的细胞迁移和侵袭。