SMAD4 and colorectal carcinoma: Papageougis et al. [28] found that loss of function of Smad4 and retention of intact TGF-β receptors could synergistically increase the levels of VEGF, enhanced migration of CRC cells with a corresponding increase in matrix metalloprotease-9 enhanced hypoxia-induced GLUT1 expression, increased aerobic glycolysis, and resistance to 5′-fluoruracil-mediated apoptosis.