Thbs4, or thrombospondin 4, is an extracellular matrix protein. It plays roles in various biological processes, such as regulating cellular attachment dynamics and extracellular matrix protein production. It is associated with pathways like FAK/PI3K/AKT, and is important in understanding tumor development, wound healing, and cardiac function [1,3,6]. Genetic models, including KO/CKO mouse models, are valuable for studying its functions.

In cancer research, Thbs4 has been found to promote the progression of multiple cancers. In hepatocellular carcinoma (HCC), its overexpression mediates cell proliferation and metastasis both in vitro and in vivo, regulating EMT progression and interacting with ITGB1 via the FAK/PI3K/AKT pathway [1]. In gastric cancer, it stimulates cell proliferation and metastasis, and may have a positive correlation with KLF9 expression [2]. In prostate cancer, overexpression of Thbs4 promotes self-renewal and proliferation of cancer stem cells by activating the PI3K/Akt pathway, while its silencing exhibits suppressive effects [4]. In colorectal cancer, PDGFRβ-associated Thbs4 may contribute to tumor development [5]. In addition, in Duchenne muscular dystrophy mouse models, increased Thbs4 expression was observed in areas of muscle fibrosis [7].

In conclusion, Thbs4 is crucial in various biological processes and disease conditions, especially in cancer development and muscle fibrosis. Studies using gene knockout or conditional knockout mouse models have significantly contributed to understanding its role in promoting cancer cell proliferation, metastasis, and its association with specific signaling pathways. This knowledge provides potential therapeutic targets for treating related diseases.