ANRIL is associated with the survival rate of patients with colorectal cancer, and affects cell migration and invasion invitro.

Abstract

Antisense noncoding RNA in the INK4 locus (ANRIL) has been reported to be upregulated in various types of human cancer, and is also highly expressed in normal human tissue. The aim of the present study was to identify whether ANRIL may be a possible target for colorectal cancer (CRC) therapy. Reverse transcription‑quantitative polymerase chain reaction was used to quantify the expression levels of the long noncoding RNA (lncRNA) ANRIL in 97paired CRC and adjacent non‑neoplastic tissue samples. In addition, the HT29 and RKO human CRC cell lines underwent ANRIL RNAinterference, and knockdown efficiency was evaluated by western blotting. Cell viability, and migratory and invasive ability were subsequently assessed. The CRC tissues were revealed to express higher levels of ANRIL lncRNA compared with the adjacent non‑neoplastic tissues (P<0.05). Furthermore, high ANRIL expression was significantly associated with reduced survival rate (P<0.05). ANRIL gene expression was successfully silenced in human CRC cells. ANRIL knockdown decreased proliferation, inhibited migration and invasion, and reduced the colony‑forming ability of the cells. These data indicated that the lncRNA ANRIL is upregulated in CRC tissues, and is associated with CRC cell pathogenesis. Furthermore, the underlying mechanisms of these effects may be exploited for therapeutic benefit.