Ltbr, short for lymphotoxin β receptor, is a key regulator involved in multiple biological processes. It activates the non-canonical nuclear factor kappa B (NF-κB) pathway, which is crucial for immune response, cell survival, and development. Ltbr is also associated with the Wnt/β-catenin signaling pathway, influencing cell fate decisions and tissue homeostasis [1,3,4,5].

Macrophage-specific knockout of Ltbr in mouse models hinders tumor growth and prolongs survival time in lung adenocarcinoma. This is achieved by blocking the immunosuppressive activity and M2 phenotype of tumor-associated macrophages (TAMs), suggesting that Ltbr plays a role in maintaining the immunosuppressive environment in tumors [1]. In addition, in murine models of cholangiocarcinoma, the activation of the Ltbr/NIK/RELB axis promotes tumor cell proliferation, while inhibition of NIK suppresses RelB expression [2].

In conclusion, Ltbr is essential in regulating immune-related functions and cell proliferation through its associated signaling pathways. The gene knockout mouse models have revealed its significance in cancer-related processes, such as tumor growth, metastasis, and the immunosuppressive tumor microenvironment, providing potential therapeutic targets for cancer treatment.