Rnf115, also known as breast cancer-associated gene 2 (BCA2), is an E3 ubiquitin ligase. Ubiquitin ligases play crucial roles in regulating protein degradation, cellular signaling, and immune responses. Rnf115 is involved in pathways such as autophagy, immune regulation, and cell-cycle control, which are vital for maintaining cellular homeostasis and organismal health. Genetic models, like knockout (KO) mouse models, have been instrumental in studying its functions [1-10].

In KO mouse models, Rnf115 deletion alleviated acute liver injury by promoting autophagy and inhibiting the inflammatory response [1]. It also inhibited M1 type macrophage activation via NF-κB and Jnk signaling pathways. In Trex1-/-mice and STINGN153S/WT bone marrow chimeric mice, knockout of RNF115 significantly inhibited systemic inflammation and autoimmune lethality [2]. Additionally, in Rnf115-/-cells, there were changes in the trafficking of Toll-like receptors (TLRs), innate antiviral responses, and autophagosome maturation [3,4,6]. In cancer-related studies, Rnf115 deficiency inhibited the growth of gastric cancer, hepatocellular carcinoma, and lung adenocarcinoma cells, while its overexpression in thyroid carcinoma and lung adenocarcinoma promoted tumor progression [5,6,7,8,9].

In conclusion, Rnf115 plays diverse and significant roles in biological processes such as autophagy, immune regulation, and tumorigenesis. The use of Rnf115 KO mouse models has provided valuable insights into its functions in various disease areas, including liver injury, autoimmune diseases, and different types of cancers, helping to further our understanding of disease mechanisms and potentially guiding the development of new therapeutic strategies.