fig7

Figure 7. Evidence for activation of the cGMP/protein kinase G (PKG) axis by dopamine receptor-1 (D1R) in breast cancer. Increased accumulation of cGMP in MDA-MB-231 cells by DA and Fenoldopam (Fen) and inhibition of cAMP. For: forskolin (A); suppression of cell viability in MDA-MB-231 and BT-20 cells by YC-1, an activator of soluble guanylate cyclase (B); abrogation of DA-induced suppression of MDA-MB-468 cell viability by pre-incubation with a D1R antagonist SCH39166. RFU: relative fluorescence units (C); preincubation with PKG inhibitor KT5823 prevents the induction of apoptosis in SUM159 cells by Fenoldopam (D); co-incubation of Cialis, an antagonist of PDE5, with Fen augments the suppression of cell viability in SUM159 cells by Fen alone (E). Redrawn and modified^[2]. *Designates significant (P < 0.05) over control