Revisiting the roles of cAMP signalling in the progression of prostate cancer

Abstract

Prostate cancer is one of the most common cancers in men and one of the top causes of death in men worldwide. Development and function of both normal prostate cells and early-stage prostate cancer cells are dependent on the cross-talk between androgen signalling systems and a variety of other transduction pathways which drive differentiation of these cells towards castration-resistance. One such signalling pathway is the ubiquitous cAMP signalling axis which functions to activate spatially restricted pools of cAMP effectors such as protein kinase A (PKA). The importance of both PKA and cAMP in the development of prostate cancer, and their interactions with the androgen receptor, were the focus of a review by Merkle and Hoffmann in 2010. In this updated review, we revisit this topic with analysis of current PKA-related prostate cancer literature and introduce novel information on the relevance of another cAMP effector, the exchange protein directly activated by cAMP (EPAC).

Metabolomics-transcriptomics joint analysis: unveiling the dysregulated cell death network and developing a diagnostic model for high-grade neuroblastoma

“…cAMP, in turn, exerts its effects on four effector proteins: exchange protein activated by cAMP, cyclic-nucleotide gated ion channels, Popeye proteins, and the cAMP-dependent PKA pathway ( 33 – 35 ). Previous studies have demonstrated the pivotal role of cAMP in various malignancies, including prostate cancer, ovarian cancer, and lung cancer ( 36 – 38 ). ADCY1 serves as a pivotal regulator of the cAMP signaling pathway and is accountable for catalyzing ATP to cAMP.…”