Cant1, short for calcium-activated nucleotidase 1, is a phosphatase and a Golgi calcium-activated nucleotidase. It preferentially hydrolyzes UDP to UMP and phosphate, and is involved in glycosaminoglycan (GAG) synthesis. Its function is crucial in pathways related to cell cycle, DNA replication, and dorso-ventral axis formation [1,2,3]. Understanding Cant1 is of great biological importance, especially regarding its role in tumorigenesis and skeletal development. Mouse models have been valuable for studying its function [4].

In mouse models of Desbuquois dysplasia type 1, Cant1 knockout (KO) mice exhibit skeletal defects such as short stature, thoracic kyphosis, and delta phalanx. The GAG content and extracellular matrix space are reduced in growth plate cartilage, and chondrocyte differentiation is impaired [4]. These findings suggest that Cant1 is essential for normal skeletal development and chondrocyte function. Additionally, in vitro experiments with lung adenocarcinoma cells show that knockdown of Cant1 leads to decreased cell proliferation, invasion, and G1 phase cell-cycle arrest [3].

In conclusion, Cant1 is vital for GAG synthesis and chondrocyte differentiation in cartilage, as demonstrated by KO mouse models of Desbuquois dysplasia. In the context of cancer, especially lung adenocarcinoma, Cant1 appears to play a role in promoting cell proliferation and invasion. Research on Cant1 using mouse models has provided insights into skeletal development-related diseases and tumorigenesis, which may contribute to the development of new treatment strategies [3,4].