MicroRNA-194 Inhibits the Epithelial–Mesenchymal Transition in Gastric Cancer Cells by Targeting FoxM1

Aim 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. Methods The expression level of miR-194 was examined using real-time PCR in human gastric cancer and noncancerous gastric ti...

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Bibliographic Details
Published in:Digestive diseases and sciences 2014-09, Vol.59 (9), p.2145-2152
Main Authors: Li, Zhenjun, Ying, Xiaojiang, Chen, Hongliang, Ye, Pingjiang, Shen, Yi, Pan, Weihuo, Zhang, Lihua
Format: Article
Language:English
Subjects:
Biochemistry
Cancer
Cancer cells
Cell Line, Tumor
Cell Movement
Comparative analysis
Development and progression
Epithelial Cells
Epithelial-Mesenchymal Transition - genetics
Forkhead Box Protein M1
Forkhead Transcription Factors - genetics
Forkhead Transcription Factors - metabolism
Gastric Mucosa - metabolism
Gastroenterology
Gene Expression Regulation, Neoplastic
Health aspects
Hepatology
Humans
Medicine
Medicine & Public Health
MicroRNA
MicroRNAs - genetics
MicroRNAs - metabolism
MicroRNAs - physiology
Oncology
Original Article
Phenotype
RNA Interference
Stem cells
Stomach cancer
Stomach Neoplasms - genetics
Stomach Neoplasms - metabolism
Transplant Surgery
Up-Regulation
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Summary:Aim 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. Methods 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. Results 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. Conclusion 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.
ISSN:0163-2116
1573-2568
DOI:10.1007/s10620-014-3159-6