Dlc1, also known as Deleted in liver cancer-1, is a potential tumor suppressor. 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. It is involved in multiple signal pathways related to cancer cell growth, apoptosis, migration, and invasion, and thus is of great importance in cancer-related biological processes [1,2].

In 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 such as clinical stage and histologic grade, and positively correlated with patient survival. Low-expression Dlc1 group was enriched in metabolic pathways, while the high-expression group was enriched in tumor immune-related activities. Dlc1 also played a key role in mediating immune cell infiltration [4]. In lung adenocarcinoma, overexpressing Dlc1 significantly inhibited cell proliferative, migratory, and invasive abilities by suppressing the MAPK/ERK signaling pathway, while knockdown of Dlc1 promoted these abilities [5].

In conclusion, Dlc1 functions as a tumor suppressor through regulating Rho signaling and other pathways, playing important roles in cancer-related biological processes. Studies using gene knockout mouse models have revealed its dispensability in maintaining normal liver and kidney function in mice, as well as its significance in cancer-related phenotypes such as tumor cell proliferation, migration, invasion, and immune cell infiltration in endometrial and lung adenocarcinoma. These findings contribute to understanding the role of Dlc1 in specific disease areas, especially in cancer, and may provide potential targets for cancer treatment.