SH3BP1, also known as ARHGAP43, belongs to the RhoGAP family. It is an important regulator involved in multiple cellular processes. SH3BP1 specifically inactivates Rac1 and its target proteins like Wave2/WAVE2, and is associated with pathways related to cell motility, such as the Ral/exocyst and Rac signaling pathways. It plays a significant role in various biological processes including cell migration, epithelial junction formation, and is also relevant in disease-related contexts like cancer progression [1,3,5,6,7,8].

In melanoma, overexpression of SH3BP1 promoted cell proliferation, migration, and invasion through the Rac1/Wave2 signaling pathway [1]. In acute myeloid leukemia, higher SH3BP1 expression was associated with poor prognosis, and down-regulation of its expression inhibited cell proliferation [2]. In cervical cancer, SH3BP1 overexpression promoted invasion, migration, and chemoresistance via the Rac1/Wave2 pathway [3]. In chronic myeloid leukemia, interactions among Cobll1, PACSIN2, and SH3BP1 regulated drug resistance, with SH3BP1 promoting the SH3BP1/Rac1 pathway to suppress tyrosine kinase inhibitor-mediated apoptosis [4]. In hepatocellular carcinoma, SH3BP1 overexpression was associated with vascular invasion, and it promoted tumor invasion and microvessel formation through the Rac1-WAVE2 signaling, contributing to metastasis and recurrence [6].

In conclusion, SH3BP1 is a crucial regulator in multiple biological processes and disease conditions, especially in various cancers. Its role in activating or inactivating key signaling pathways like Rac1/Wave2 has been demonstrated through various in-vivo and functional studies. Understanding SH3BP1's functions may provide new therapeutic targets for treating related diseases, such as melanoma, acute myeloid leukemia, cervical cancer, chronic myeloid leukemia, and hepatocellular carcinoma.