The role of miRNA and lncRNA in gastric cancer

Abstract

Gastric cancer is one of the most common cancers and has the highest mortality rate worldwide. It is worthwhile to explore the mechanism of gastric cancer progression. An increasing number of studies have found that non-coding RNAs including miRNA and lncRNA play important roles in gastric cancer progression. This review summarized the role of ectopic miRNA in gastric cancer proliferation, growth, migration, invasion and apoptosis. Meantime, aberrantly expressed miRNA also received a great deal of attention as potential biomarker for gastric cancer diagnosis and therapy. Over the last decade, lncRNA was considered to regulate gastric cancer progression at the transcript and post-transcript level. At the transcript level, lncRNA induced gastric cancer progression by changing chromatin modification and mRNA stabilization to regulate mRNA and miRNA expression. Furthermore, lncRNA regulated gastric cancer progression by completely combining with miRNA to produce ceRNA or promote protein stabilization at the post-transcript level. Greater attention of miRNA and lncRNA in gastric cancer can provide new insight of mechanism of cancer development and may be acted as a new anticancer target.

Keywords: gastric cancer; lncRNA; miRNA.

Figure 1. lncRNA regulates gene expression at the transcriptional level

(A) HOXA11-AS binds to several RNA binding proteins (PRC2, LSD1 and DNMT1) and function as a scaffold to inhibit PRSS8 and KLF2 at the transcriptional level to promote gastric cancer proliferation and invasion. (B) HOTAIR binding to PRC2 significantly inhibited miR-34a expression at the transcript level ultimately activating HGF/c-met signaling to promote EMT.

Figure 2. lncRNA regulates gene expression at the transcriptional level

(A) lncRNA BC032469 functions as a ceRNA to sponge for miR-1207-5p, promoting hTERT expression to induce gastric cancer cell proliferation and metastasis. (B) FOXM1 induced lncRNA PVT1 expression at the transcriptional level. Then PVT1 binds to FOXM1 protein to increase its stabilization, forming a positive feedback loop and promoting gastric cancer cell proliferation and metastasis.