TRIM59, a member of the tripartite motif containing (TRIM) protein family, functions as an E3 ubiquitin ligase through its RING domain. It is involved in development, immune response, and the invasion and metastasis of tumors, and is expressed by multiple types of cells. It participates in pathways such as the NFKB pathway and is associated with autophagy, macrophage activation, and cell proliferation-related processes [1].

Macrophage-specific TRIM59 conditional knockout (CKO) mice have revealed that TRIM59 deficiency promotes M1 macrophage activation and inhibits colorectal cancer through the STAT1 signaling pathway. TRIM59 could regulate macrophage polarization by ubiquitinating and degrading STAT1 [2].

In summary, TRIM59 is significant in immune-related processes and tumor-related events. The use of CKO mouse models has provided insights into its role in colorectal cancer, suggesting that the TRIM59/STAT1 signaling pathway may be a promising target for CRC treatment. Manipulating TRIM59 levels and activity could potentially be an avenue for treating immune diseases and tumors [1,2].

References:

1. Jin, Zheng, Chen, Tiffany, Zhu, Zhenhua, Xu, Baohui, Yan, Dongmei. 2022. The role of TRIM59 in immunity and immune-related diseases. In International reviews of immunology, 43, 33-40. doi:10.1080/08830185.2022.2102618. https://pubmed.ncbi.nlm.nih.gov/35975813/

2. Wang, Haidong, Lou, Jun, Liu, Hao, Pan, Hongming, Han, Weidong. 2024. TRIM59 deficiency promotes M1 macrophage activation and inhibits colorectal cancer through the STAT1 signaling pathway. In Scientific reports, 14, 16081. doi:10.1038/s41598-024-66388-0. https://pubmed.ncbi.nlm.nih.gov/38992114/