RhoA regulates actin cytoskeleton but recent evidence suggest a role for this 
conserved Rho GTPase also in other cellular processes, including transcriptional 
control of cell proliferation and survival. Interestingy, loss of RhoA is 
synthetic lethal with oncogenic Myc, a master transcription factor that turns on 
anabolic metabolism to promote cell growth in many cancers. We show evidence 
indicating that the synthetic lethal interaction between RhoA loss and Myc 
arises from deficiency in glutamine utilization, resulting from impaired 
co-regulation of glutaminase expression and anaplerosis by Myc and RhoA - serum 
response factor (SRF) pathway. The results suggest metabolic coordination 
between Myc and RhoA/SRF in sustaining cancer cell viability and indicate 
RhoA/SRF as a potential vulnerability in cancer cells for therapeutic targeting.