Trim13-induced ubiquitination of RPS27A inhibits the progression of lung cancer by depending on the inactivation of NF-κB signaling pathway.

Abstract

Lung cancer (LC) is the leading cause of cancer-related death worldwide. Recent studies have shown that tripartite motif 13 (TRIM13) play important regulatory roles in the progression of different tumors. In this study, we focused on the role of TRIM13 in LC tumorigenesis and its underlying molecular mechanisms. The study demonstrated TRIM13 was identified as a novel tumor suppressor gene of LC and its overexpression suppressed LC progression in vitro and in vivo. Mechanistically, TRIM13 interacted with RPS27A, increasing RPS27A ubiquitination and degradation. Furthermore, RPS27A overexpression reversed the inhibitory effect of TRIM13 overexpression on LC progression. By binding to RPS27A and encouraging its ubiquitination and degradation, TRIM13 hindered LC advancement. We also found that RPS27A overexpression reversed the inhibitory effect of TRIM13 overexpression on NF-κB signaling, thereby further promoting the proliferation and metastasis of LC cell lines. Therefore, targeting the TRIM13/RPS27A/NF-κB signaling axis may be a promising target for LC treatment.