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2017 ; 7
(7
): 905-914
Nephropedia Template TP
gab.com Text
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English Wikipedia
miR-944 inhibits metastasis of gastric cancer by preventing the
epithelial-mesenchymal transition via MACC1/Met/AKT signaling
#MMPMID28680805
Pan T
; Chen W
; Yuan X
; Shen J
; Qin C
; Wang L
FEBS Open Bio
2017[Jul]; 7
(7
): 905-914
PMID28680805
show ga
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. Reduced expression of mi-944 was also observed in GC cell
lines. 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. We also found that the Met-AKT pathway might be involved in
MACC1-mediated EMT. 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.