Rassf10, a member of the Ras-association domain family, is a tumor suppressor gene [1-10]. It contains a RA (Ras-association) and two coiled domains, and is involved in multiple biological processes, such as regulating cell cycle, apoptosis, and cell invasion. It is associated with pathways like Wnt/β-catenin, PI3K-AKT, MAPK, and calcium signaling [2-4, 7].

In mouse models, Rassf10 haploinsufficiency promotes neoplasia formation. Rassf10-/-and p53-deficient mice show a three-fold increased rate of kidney cysts compared with p53-/-controls, indicating its role in kidney-related diseases [2]. In various cancers, loss-of-function studies have shown significant effects. For example, in esophageal squamous cell carcinoma, its overexpression reduces cell growth, colony formation, migration, and invasion, and mediates inactivation of the Wnt/β-catenin pathway [1]. In lung cancer cell lines, its epigenetic inactivation is common, and restoring its expression induces apoptosis [3].

In conclusion, Rassf10 functions as a tumor suppressor. Gene knockout mouse models have been crucial in revealing its role in promoting neoplasia in kidney-related diseases and its significance in multiple cancer types, including lung, esophageal, and colorectal cancers. Understanding Rassf10 can provide new insights into cancer development mechanisms and potential therapeutic targets.