YES1, a nonreceptor tyrosine kinase, belongs to the SRC family of kinases (SFK) [1,2,5]. It controls multiple cancer-related signaling pathways, and is of great biological importance in tumorigenesis. YES1 is involved in pathways promoting cell proliferation, survival, invasion, and angiogenesis during cancer development [2]. Genetic models, such as gene knockout (KO) or conditional knockout (CKO) mouse models, could potentially be used to further study its functions.

Genetic depletion of YES1 in in vitro and in vivo models significantly reduced cell proliferation, three-dimensional organoid formation, tumor growth, and distant metastasis, leading to extensive apoptosis and tumor regressions in small-cell lung cancer (SCLC) [4]. In triple-negative breast cancer (TNBC), disrupting YES1, either genetically or pharmacologically, induced aberrant mitosis, centrosome amplification, multipolar spindles, and chromosomal instability [6]. In gastric cancer, knockdown of YES1 decreased cell invasion and migration in vitro and tumor growth in mouse models [3].

In conclusion, YES1 plays a pivotal role in promoting cancer cell proliferation, survival, and invasiveness across various cancer types, as revealed through model-based research. The use of KO/CKO mouse models in these studies has provided insights into the role of YES1 in SCLC, TNBC, and gastric cancer, suggesting that targeting YES1 could be a promising strategy for cancer treatment [1,3,4,6].