Abstract
BackgroundThe objective of this study was to investigate the role and mechanism of long non-coding RNA MIAT in gastric cancer (GC).MethodsReal-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.ResultsMIAT 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.ConclusionsOur data indicated that MIAT played an oncogenic role in GC growth and metastasis, and could serve as a novel molecular target for treating GC.
Highlights
The objective of this study was to investigate the role and mechanism of long non-coding RNA Myocardial infarction associated transcript (MIAT) in gastric cancer (GC)
MIAT was up-regulated in GC tissues and cell lines To determine MIAT expression in gastric cancer tissues, we performed realtime PCR in gastric cancer tissue specimens and matched adjacent normal tissues
MIAT was pulled down by miR-141, while the introduction of mutations which disrupted the predicted miRNA recognition sites between MIAT and miR-141 resulted in the inability of miR-141 to pull down MIAT (Fig. 5d). These results indicated that MIAT acted as miR-141 sponge in GC cells
Summary
The objective of this study was to investigate the role and mechanism of long non-coding RNA MIAT in gastric cancer (GC). Proliferation and metastasis are two important factors which are closely linked with poor prognosis and death in GC [2, 3]. Molecules closely related to cell proliferation and metastasis. The DEAD-box RNA helicase 5 (DDX5), an ATPdependent DEAD-box RNA helicase, acts as a transcriptional co-activator of several cancer-associated transcription factors and plays an important role in transcription initiation [5]. DDX5 is overexpressed in a variety of tumors and contributes to promoting cancer cell proliferation and metastasis [6, 7].
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