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Long non-coding RNA MIAT promotes gastric cancer growth and metastasis through regulation of miR-141/DDX5 pathway.

Long non-coding RNA MIAT promotes gastric cancer growth and metastasis through regulation of miR-141/DDX5 pathway.
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Sha M, Lin M, Wang J, Ye J, Xu J, Xu N, Huang J,


Sha M, Lin M, Wang J, Ye J, Xu J, Xu N, Huang J, (click to view)

Sha M, Lin M, Wang J, Ye J, Xu J, Xu N, Huang J,

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Journal of experimental & clinical cancer research : CR 2018 03 1437(1) 58 doi 10.1186/s13046-018-0725-3

Abstract
BACKGROUND
The objective of this study was to investigate the role and mechanism of long non-coding RNA MIAT in gastric cancer (GC).

METHODS
Real-time PCR was used to determine MIAT level in 120 GC tissues, and in two gastric cancer cell lines. The clinicopathological characteristics of MIAT in GC patients were analyzed. Small interfering RNA specific for MIAT (si-MIAT) and lentivector for si-MIAT was performed to down-regulate MIAT expression in GC cells and in animal tumor model, respectively. The interaction of MIAT and miR-141 was measured by RNA pull-down assay and RNA immunoprecipitation. The biological function of si-MIAT on GC cell growth and metastasis were explored through flow cytometry assay, invasion and migration assay in vitro.

RESULTS
MIAT was highly expressed in GC tissues and cell lines and correlated with differentiation degree, TNM stage, distant metastasis, and lymph node metastasis. MIAT knockdown inhibited GC growth and metastasis both in vitro and in vivo. Furthermore, MIAT acted as miR-141 sponge and regulated its target gene DDX5 expression. In BGC-823 and MGC-803 cells with si-MIAT, DDX5 overexpression resulted in an increase of cell proliferation, migration and invasion.

CONCLUSIONS
Our data indicated that MIAT played an oncogenic role in GC growth and metastasis, and could serve as a novel molecular target for treating GC.

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