The role of MALAT-1 in the invasion and metastasis of gastric cancer.

OBJECTIVES

The long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT-1) has been reported to be over-expressed in several cancer types. However, its role in gastric cancer (GC) remains unclear. In the present study, we examined the expression of MALAT-1 in GC cells and tissues and explored its role in GC cell migration and invasion.

MATERIALS AND METHODS

Real-time quantitative polymerase chain reaction (qRT-PCR) was used to analyze the expression level of MALAT-1 in six GC cell lines and 20 gastric tissues (20 GC and 20 adjacent normal mucosa). Functional characterization for the role of MALAT-1 in GC was performed by small interfering RNA (siRNA) knockdown, followed by series of in vitro and in vivo experiments.

RESULTS

MALAT-1 was upregulated in GC cell lines and tissues compared with the immortalized gastric epithelial cell line GES and adjacent normal tissues, respectively. Moreover, MALAT-1 expression was higher in the high-metastatic-potential GC cell line SGC7901M than in the low-metastatic-potential GC cell line SGC7901NM. In vitro and in vivo assays showed that siRNA-mediated silencing of MALAT-1 inhibited GC cell migration and invasion. In addition, suppressing MALAT-1 expression resulted in a decrease in the expression of the Epithelial-mesenchymal transition (EMT)-associated marker vimentin and an increase in the expression of E-cadherin at both the mRNA and protein levels.

CONCLUSIONS

MALAT-1 may promote the migration and invasion of GC cells in part by regulating EMT.