TRIM52 regulates the proliferation and invasiveness of lung cancer cells via the Wnt/β‑catenin pathway.

Abstract

As a major cause of cancer‑associated mortalities, lung cancer is frequently diagnosed in males and females with an incidence ratio of 2.1:1. Tripartite motif 52 (TRIM52), an E3 ubiquitin ligase, has been reported to be involved in various biological functions, including cell proliferation and invasiveness. In the present study, an elevated TRIM52 level was observed in tumor tissues of patients with lung cancer and in lung cancer cell lines. The downregulation of TRIM52 in lung cancer cells significantly suppressed the proliferation of lung cancer cells, arrested the cell cycle at the G1 phase and was accompanied by a decrease in the levels of β‑catenin, proliferating cell nuclear antigen, c‑Myc and Cyclin D1 proteins. Additionally, TRIM52‑induced cell proliferation and invasiveness, as well as the levels of cell cycle‑associated proteins, were completely counteracted by the Wnt/β‑catenin inhibitor XAV939. Based on these data, it was speculated that TRIM52 is critical for lung cancer progression and that downregulation of TRIM52 could inhibit cell proliferation by blocking cell cycle progression. It was also speculated that TRIM52 upregulation promotes proliferation and invasiveness through activation of the Wnt/β‑catenin pathway. Thus, TRIM52 has the potential to be a therapeutic target for lung cancer.