Fig. 7: Schematic of the proposed mechanism by which PDE4DIP promotes lung cancer cell growth.
From: The PDE4DIP-AKAP9 axis promotes lung cancer growth through modulation of PKA signalling

In NSCLC cells expressing high levels of PDE4DIP, the formation of the PDE4DIP-AKAP9-PKA RIIα complex at the Golgi apparatus increases the stability of PKA RIIα, resulting in PKA inactivation. Knockdown of PDE4DIP promotes the ubiquitination-mediated degradation of PKA RIIα, thereby releasing active PKA catalytic subunits, enhancing CREB phosphorylation, and leading to the expression of downstream target genes related to apoptosis and cell cycle arrest.