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

Abstract

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.

Keywords:

• LncRNA
• MALAT-1
• gastric cancer
• metastasis
• EMT

Acknowledgements

The authors thank State Key Laboratory of Cancer Biology and Xijing Hospital of Digestive Diseases (Xi’an, China) for providing specimens. This work was supported by the National Natural Science Foundation of China under Grant numbers [81272349 and 81301804].

Disclosure statement

The authors report no conflicts of interest.

Additional information

Funding

This work was supported by the National Natural Science Foundation of China under Grant numbers [81272349 and 81301804].