Fig 1: DLX1 is a critical downstream effector of FOXM1 that activates TGF-ß1/SMAD4 signaling. (a) The western blot analysis showed increased expression of two TGF-ß signaling targets, PAI-1 and JUNB, in SKOV3 cells stably expressing DLX1 (SK-C2) in response to TGF-ß1 (5 ng/ml) treatment compared with the vector control (SK-vector). (b) DLX1 induced a concentration-dependent increase in PAI-1 luciferase activity upon TGF-ß1 treatment (10 ng/ml, 3 h). (c) Depletion of DLX1 by lentiviral shRNA approach remarkably reduce the expressions of PAI-1 and JUNB in OVCA433 and SKOV3 cells upon treatment of TGF-ß1 (5 ng/ml) for 5 h. (d) FOXM1 knockdown does not alter the ability of DLX1 to upregulate PAI-1 and JUNB expression upon TGF-ß1 (5 ng/ml) treatment in a SKOV3 cell model stably expressing DLX1 (SK-C2). (e) The western blot analysis showed that SMAD4 knockdown markedly attenuated TGFß1-induced expression of PAI-1 and JUNB, with or without stably overexpressing DDK/DLX1 in SKOV3 cells (SK-C2 and empty vector control).