miR-944 inhibits metastasis of gastric cancer by preventing the epithelial-mesenchymal transition via MACC1/Met/AKT signaling.MicroRNAs (miRNAs) are reported to play vital roles in tumor progression.  Recently, miR-944 was reported to play either an oncogenic or tumor suppressive role in human cancers.  However, the expression of miR-944 and its exact role in gastric cancer (GC) remain unknown.  This study aimed to evaluate whether loss of miR-944 could promote the epithelial-mesenchymal transition (EMT) of GC.  Reduced expression of miR-944 was identified in 40 pairs of human GC and matched normal tissues by qRT-PCR.  Restoration of miR-944 inhibited cell migration and invasion in MGC-803 cells, while its loss facilitated metastasis of SGC-7901 and BGC-823 cells.  Notably, miR-944 overexpression prohibited EMT of GC cells in vitro, while miR-944 knockdown had the opposite effect.  Bioinformatics software predicted that MACC1 was a direct target of miR-944.  We observed negative regulation of miR-944 on MACC1 expression, and direct binding between miR-944 and MACC1 was verified by dual-luciferase assays in HEK293T cells.  Restoration of MACC1 resulted in promoted EMT and metastasis in miR-944-overexpressing MGC-803 cells.  Loss of MACC1 abrogated the effects of miR-944 knockdown on EMT and metastasis of SGC-7901 cells.  In conclusion, miR-944 acts as an inhibitor of EMT and metastasis of GC by targeting MACC1.  This study highlights the potential effects of miR-944 in the prognosis and treatment of GC.
miR-944
Bioinformatics software predicted that MACC1 was a direct target of miR-944. 
Bioinformatics software
Reduced expression of miR-944 was identified in 40 pairs of human GC and matched normal tissues by qRT-PCR. 
qRT-PCR