RhoC is a small GTPase that regulates cell migration, cytoskeletal dynamics, and cytokinesis through nucleotide-dependent signaling. Primary functions include controlling actin stress fiber assembly, focal adhesion formation, and myosin-dependent contractile ring formation during cell division 1. RhoC activation occurs through multiple mechanisms: direct interaction with BCAT1 and stimulation by branched-chain α-keto acids 2, non-degrading ubiquitination by E3 ligase LNX1 (suppressed by LIS1) 3, and spatial regulation via p190RhoGEF/p190RhoGAP complexes 4. Unlike RhoA which regulates contractility or RhoB which localizes to endosomes, RhoC specifically promotes cell locomotion and invasive protrusions including invadopodia and lamellipodia 5, 6. RhoC dysregulation associates with multiple cancers through enhanced cell migration and metastasis. Expression increases in relapsed prostate cancer following radiation therapy, suggesting treatment resistance mechanisms 7. In adult T cell leukemia, RhoC overexpression (as a miR-455-3p target) activates oncogenic pathways including Myc targets and sphingomyelin-mediated lipid metabolism 8. Targeting RhoC activity through BCAT1 inhibition (candesartan) suppresses cancer cell motility and peritoneal metastasis 2, indicating therapeutic potential. RhoC represents a RhoA/RhoB-specific regulatory module and a candidate biomarker and therapeutic target in metastatic disease.