RP11‑619L19.2 promotes colon cancer development by regulating the miR‑1271‑5p/CD164 axis.

Abstract

Colon cancer (CC) is one of the leading causes of cancer-related mortality in China and western countries. Several studies have demonstrated that long non-coding RNAs (lncRNAs) play critical roles in cancer development. However, the function of lncRNA RP11-619L19.2 in colon cancer remains unclear. The aim of the present study was to investigate the expression pattern, function and underlying mechanism of action of RP11-619L19.2 in CC development and metastasis. RP11-619L19.2 was found to be highly expressed in CC tissues and cell lines, and it was associated with advanced TNM stage and lymph node metastasis. Furthermore, knockdown of RP11-619L19.2 inhibited CC cell proliferation, migration, invasion and epithelial-to-mesenchymal transition (EMT). It was also observed that RP11-619L19.2 was reciprocally repressed by miR-1271-5p. Of note, miR-1271-5p negatively regulated CD164 expression by directly targeting the 3′-untranslated region of CD164. Overexpression of CD164 reversed the antimetastatic activity of RP11-619L19.2 knockdown in CC cells. Mechanistically, it was demonstrated that lncRNA RP11-619L19.2 played an oncogenic role and promoted CC development and metastasis by regulating the miR-1271-5p/CD164 axis and EMT. In conclusion, the findings of the present study indicated that RP11-619L19.2 regulates CD164 expression and EMT by sponging miR-1271-5p, which may provide novel targets for lncRNA-directed diagnosis and therapy for patients with CC.