The expression of long non-coding RNA LINC01389, LINC00365, RP11-138J23.1, and RP11-354K4.2 in gastric cancer and their impacts on EMT

Abstract

Background

Epithelial cancers acquire the epithelial to mesenchymal transition (EMT), which leads tumor cells to invade and metastasize to adjacent and distant tissues. The mechanisms involved in EMT phenotype are controlled by numerous markers as well as signalling pathways. Recently, long non-coding RNAs (lncRNAs) were introduced that play the regulatory role in EMT via crosstalk with EMT-related transcription factors and signalling pathways. The present study aimed to investigate the expression of four lncRNAs in human GC and elucidate their probable role in EMT procedure and the pathogenesis of gastric cancer (GC).

Methods

The expression profile of lncRNAs (LINC01389, LINC00365, RP11-138J23.1, and RP11-354K4.2) and mRNAs (TWIST1, MMP13, MAML1, CD44s, and SALL4) between eighty-three GC and adjacent non-cancerous tissues were assessed by quantitative real-time PCR.

Results

The significant downregulation of LINC00365 (66.3%) and RP11-354K4.2 (62.7%) were observed in GC samples; while the upregulation of LINC01389, RP11-138J23.1, TWIST1, MMP13, MAML1, CD44s, and SALL4 were found in 67.5%, 45.8%, 56.6%, 44.6%, 59%, 55.4%, and 62.7% tumors samples at the mRNA level, respectively. Dysregulation of these lncRNAs and EMT-related markers was significantly related to each other in a variety of clinicopathological features of patients (P < 0.05), indicating positive correlations between LINC01389, LINC00365, RP11-138J23.1, and RP11-354K4.2 with EMT status in GC.

Conclusion

These EMT-regulating lncRNAs may play a key role in transforming gastric epithelial to mesenchymal phenotype and can be novel therapeutic targets for GC. Our results highlight the importance of discovering new lncRNAs involved in gastric carcinogenesis. Detailed molecular mechanisms of these noncoding-coding markers in GC are urgently required.