Arhgef38, short for Rho guanine nucleotide exchange factor 38, is related to tumor cell polarization. It participates in the tumor cell metastasis pathway and might play a role in cell invasion and migration processes, which are crucial in cancer development [1,3].

In prostate cancer (PCa), Arhgef38 is significantly up-regulated compared to benign prostatic hyperplasia, and its expression is higher in high-grade PCa and those with higher Gleason scores, indicating its potential as a biomarker for aggressive PCa [1]. Silencing Arhgef38 in PCa cells suppresses their proliferation, migration, and invasiveness, suggesting it may serve as an oncogene in PCa [3].

In breast cancer, a low-frequency missense variant rs61751053 in ARHGEF38 is associated with overall breast cancer risk in women of African ancestry [2].

In the context of infective endocarditis, the type IV collagen-Cnm-ARHGEF38 pathway may play a crucial role, as knockdown of ARHGEF38 strongly reduces human umbilical vein endothelial cell invasion by Cnm-positive Streptococcus mutans [4].

In summary, Arhgef38 is closely associated with cancer-related processes, especially in prostate and breast cancers, and may also be involved in the pathogenesis of infective endocarditis. The functional studies on Arhgef38, such as knockdown experiments in PCa cells, have provided valuable insights into its role in disease development, highlighting its potential as a therapeutic target or biomarker.