Trim30a, a member of the tripartite motif-containing protein family, is involved in multiple biological functions. It has been associated with immune-related pathways and protein quality control systems [1,3,4]. In the context of the immune system, it may act as a negative regulator of the immune response, and its role in protein quality control could potentially impact tumorigenesis and immune surveillance [1,3].

A study on murine Trim30a overexpression in tumour cells showed that it sensitises tumour cells to NK cell-mediated cytolysis. Trim30a-overexpressing tumour cells grow slower in immune-competent mice but not in NK cell-depleted mice. Mechanistically, Trim30a overexpression impairs the protein quality control system in tumour cells, increasing reactive oxygen species production induced by proteotoxic stress and reducing the expression of genes encoding proteasome subunits and antioxidant proteins. This indicates its potential as a tumour suppressor and immune modulator [1]. Another study found that Trim30a expression was increased in Sting-deficient mice infected with Helicobacter pylori, suggesting its involvement in the immune response regulation during this infection [2]. In mouse male germ cells, a testis-specific lncRNA, lncRNA-Tcam1, was shown to upregulate Trim30a, and Trim30a was identified as a negative regulator of the immune response during spermatogenesis [3].

In conclusion, Trim30a is a key gene involved in immune regulation and protein quality control. Studies using mouse models, such as overexpression in tumour cells and gene-deficient mice in infection models, have revealed its potential as a tumour suppressor and its role in the immune response during specific infections. Its regulation by lncRNA-Tcam1 in male germ cells also highlights its importance in spermatogenesis-related immune response regulation.