Abstract

Rap2, a member of the GTP-binding proteins, is widely upregulated in many types of tumors. The specific effectors of Rap2 can affect multiple cancer-associated cellular processes, including cytoskeleton reorganization, proliferation, migration, and inflammation. However, the functional role of Rap2 in tumorigenesis and the interplay between different effectors remain to be fully elucidated. A more thorough understanding of the cancer-associated signaling networks of Rap2 is expected to facilitate drug discovery targeting Rap2 for cancer therapy. The present review mainly focused on recent studies on the functional and physical interactions between Rap2 and its effectors. We also speculated on the relevance of these pathways to tumorigenesis.

Keywords: Cancer, MAP4K4, PLCε, Rap2, TNIK.

Graphical Abstract