CapG, the gelsolin-like actin-capping protein, belongs to the gelsolin superfamily. It plays a crucial role in modulating actin dynamics and actin-based motility. It is involved in multiple signaling pathways such as the Wnt/β-catenin, PI3K/AKT, and NF-κB pathways, and is of great biological importance in processes like cell migration, proliferation, and metastasis [1,2,3,4]. Genetic models, especially KO/CKO mouse models, can be valuable for studying its functions.

Knockdown of Capg in an AML murine model led to exhausted AML cells and prolonged survival of AML mice, indicating that CapG promotes AML progression through the NF-κB pathway [2]. In colorectal cancer cells, CapG knockdown blocked the cell cycle at the G1 phase and triggered apoptosis and ferroptosis by upregulating the P53 pathway, inhibiting CRC cell growth in vitro and in vivo [5]. In breast cancer, overexpressing CapG significantly enhanced paclitaxel resistance in cells and xenograft tumors, and high CapG levels correlated with shorter relapse-free survival and hyper-activation of PI3K/Akt signaling [6].

In conclusion, CapG is essential in regulating cell-related processes such as proliferation, apoptosis, and metastasis. Model-based research, especially KO/CKO mouse models, has revealed its significant role in diseases like acute myeloid leukemia, colorectal cancer, and breast cancer, providing potential therapeutic targets for these diseases.