Upregulation of long non‑coding RNA CCEPR is associated with poor prognosis and contributes to the progression of ovarian cancer through regulating the Wnt/β‑catenin signaling pathway.

Accumulating evidence has demonstrated that the expression of long non‑coding RNAs (lncRNAs) is altered in various types of cancer, which may prove beneficial for their use as biomarkers. Cervical carcinoma expressed PCNA regulatory lncRNA (CCEPR) is a recently identified lncRNA, which has an important role in regulating cell proliferation and apoptosis in cervical and bladder cancer; however, whether CCEPR is involved in the progression of ovarian cancer (OC) remains largely unclear. The aim of the present study was to determine the clinical significance of CCEPR in OC and to investigate its biological roles. Cell Counting Kit‑8 assay was used to analyze cell proliferation, Transwell assay was used to assess invasion, flow cytometric analysis was used to analyze apoptosis, and western blotting was used to perform mechanistic studies. CCEPR expression levels were significantly elevated in OC tissues compared with adjacent non‑cancer tissues. Similarly, significant increases in CCEPR expression were observed in OC cell lines (SK‑OV‑3 and OVCAR‑3) compared with the ovarian surface epithelial cell line, HOSEpiC. The increased expression levels of CCEPR were associated with increased invasion, higher International Federation of Gynecology and Obstetrics stage and a poorer overall survival rate. In vitro, the genetic silencing of CCEPR decreased the cell proliferation rate and invasive ability of OC cells, and promoted apoptosis. CCEPR‑silenced OC cells also demonstrated decreased expression levels of four proteins involved in the Wnt/β‑catenin signaling pathway: Cyclin D1, β‑catenin, Myc and matrix metallopeptidase‑7. In conclusion, the present study demonstrated that increased expression levels of CCEPR may predict poor prognosis in patients with OC and contribute to the progression of OC through regulating the Wnt/β‑catenin signaling pathway.