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Hepatitis B virus X protein (HBx) has been termed a viral oncoprotein, and is involved in the initiation and progression of hepatocellular carcinoma (HCC). Cyclooxygenase‑2 (COX‑2) and β‑catenin have been attributed to the oncogenic activity of HBx in HBV‑associated HCC. The present study aimed to determine whether there is crosstalk between COX‑2 and the Wnt/β‑catenin signaling pathway during HL‑7702‑HBx cell proliferation, and to investigate the associated underlying molecular mechanism.  In the present study, cell proliferation assay, colony formation assay and flow cytometric analysis were used to detect the proliferative ability of cells. Reverse transcription‑quantitative polymerase chain reaction and western blotting were performed to examine the mRNA and protein expression of COX‑2, β‑catenin, cyclin‑D1 and c‑myc. The results demonstrated that HL‑7702‑HBx exhibited increased cell proliferation, higher colony formation efficiency and a shortened G1 period of the cell cycle. In addition, the mRNA and protein expression levels of COX‑2 were increased, and this was associated with HL‑7702‑HBx cell growth. Furthermore, the expression of β‑catenin and its target genes, cyclin‑D1 and c‑myc proto‑oncogene protein, was upregulated by HBx via COX‑2. Finally, HBx promoted HL‑7702 cell proliferation through the Wnt/β‑catenin signaling pathway. In conclusion, the primary finding of the present study was that HBx may promote HL‑7702 cell proliferation via the COX‑2/Wnt/β‑catenin pathway. Thus, it may be helpful to further investigate the molecular mechanism of HBV‑associated hepatocellular carcinoma.

HBx promotes the proliferative ability of HL‑7702 cells via the COX‑2/Wnt/β‑catenin pathway