LncRNA CHRF promotes cell invasion and migration via EMT in gastric cancer

Long non-coding RNAs (lncRNAs) have been verified to involve in the development and progression of gastric cancer (GC). However, the expression of lncRNA CHRF level in GC has not been mentioned before. Here, we focused on the function of lncRNA CHRF played in GC.

A total of 103 GC tissues and paired para-tumor tissues from GC patients were collected. The quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was applied to measure the lncRNA CHRF level in these samples and GC cell lines. The Wound-healing experiment, transwell assay, and Matrigel assay were employed to study the migration and invasion abilities of GC cells. The underlying molecular of lncRNA CHRF was measured using Western-blot.

LncRNA CHRF expression was significantly higher in 103 GC tissue samples compared with the adjacent para-tumor samples. In GC cells, lncRNA CHRF showed increased expression levels than the human fetal gastric epithelial cells (GES-1). Inhibition of lncRNA CHRF reduced the invasion and migration of MKN-7 cells while the over-expression of lncRNA CHRF promoted HGC-27 cells metastasis. Furthermore, we found that lncRNA CHRF could promote the progression of epithelial-mesenchymal transition (EMT) to promote the GC cell metastasis.

Our current study demonstrated that lncRNA CHRF functioned as an oncogene in GC and promoted cell invasion and migration via EMT. This might furnish a potential target for the GC biological diagnosis and therapy.