Dlc1, short for Deleted in liver cancer-1, is a potential tumor suppressor gene. It acts as a GTPase-activating protein for Rho family members, negatively regulating Rho proteins by hydrolyzing their active GTP-bound state to the inactive GDP-bound state [1,2]. The regulation of Rho proteins by Dlc1 is involved in multiple cellular processes such as cell growth, colony formation, apoptosis, senescence, autophagy, migration, and invasion, which are crucial for normal cell function and disease prevention [1].

In a study on endothelial cell-specific Dlc1 knockout mice, no histological or clinical difference was found between knockout and wild-type mice up to 24 months of age, indicating that lack of endothelial Dlc1 alone does not compromise kidney and liver function in mice [3]. In endometrial carcinoma, Dlc1 expression negatively correlated with clinical characteristics like clinical stage and histologic grade, and positively correlated with patient survival. It also played a key role in mediating immune cell infiltration, suggesting its importance in tumor microenvironment remodeling [4]. In acute myeloid leukemia, low levels of Dlc1 were detrimental to the long-term prognosis of patients [5].

In conclusion, Dlc1 is a significant tumor suppressor gene regulating Rho signaling and various cellular processes. Studies using gene knockout mouse models have provided insights into its non-essential role in endothelial-related liver and kidney functions, as well as its importance in endometrial carcinoma prognosis and immune cell infiltration, and acute myeloid leukemia prognosis. These findings contribute to understanding its biological functions and potential applications in cancer treatment.