RP11‑619L19.2 promotes colon cancer development by regulating the miR‑1271‑5p/CD164 axis
- Xin‑Wu Zhang
- Shun‑Le Li
- Di Zhang
- Xiao‑Li Sun
- Hong‑Jun Zhai
Affiliations: Department of General Surgery, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710004, P.R. China
- Published online on: October 7, 2020 https://doi.org/10.3892/or.2020.7794
Copyright: © Zhang
et al. This is an open access article distributed under the
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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.