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2015 ; 6
(11
): e2000
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MicroRNA-22 inhibits tumor growth and metastasis in gastric cancer by directly
targeting MMP14 and Snail
#MMPMID26610210
Zuo QF
; Cao LY
; Yu T
; Gong L
; Wang LN
; Zhao YL
; Xiao B
; Zou QM
Cell Death Dis
2015[Nov]; 6
(11
): e2000
PMID26610210
show ga
MicroRNAs (miRNAs) deregulation is frequent in human gastric cancers (GCs), but
the role of specific miRNAs involved in this disease remains elusive. MiR-22 was
previously reported to act as tumor suppressors or oncogenes in diverse cancers.
However, their accurate expression, function and mechanism in GC are largely
unclear. Here, we found that the expression of miR-22 was significantly reduced
in clinical GC tissues compared with paired adjacent normal tissues, and was
significantly correlated with a more aggressive phenotype of GC in patients, and
miR-22 low expression correlated with poor overall survival. The introduction of
miR-22 markedly suppressed GC cell growth, migration and invasion, and inhibition
of miR-22 promoted GC cell proliferation, migration and invasion in vitro. We
further demonstrated that miR-22 acted as tumor suppressors through targeting
extracellular matrix (ECM) remodeling member matrix metalloproteinase 14 (MMP14)
and epithelial-to-mesenchymal transition (EMT) inducer Snail in GC. Moreover,
ectopic expression of MMP14 or Snail restored inhibitory effects of miR-22 on
cell migration and invasion in GC cells, and a negative relationship between the
miR-22 expression and MMP14 or Snail mRNA levels was observed in GC. Finally,
overexpression of miR-22 suppressed tumor growth, peritoneal dissemination and
pulmonary metastasis in vivo. Taken together, we identified that miR-22 is a
potent tumor suppressor in GC. MiR-22 downregulation promotes GC invasion and
metastasis by upregulating MMP14 and Snail, and then inducing ECM remodeling and
EMT. These findings provide a better understanding of the development and
progression of GC and may be an important implication for future therapy of the
GC.
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