FABP5 as a novel molecular target in prostate cancer

Abstract

Emerging evidence suggests that dysregulated lipid signaling is a key factor in prostate cancer (PC), through fatty acid activation of the nuclear receptors peroxisome proliferator-activated receptors (PPARs), leading to the upregulation of protumoral genes. Fatty acid-binding proteins (FABPs) are intracellular lipid-binding proteins that transport fatty acid to PPARs, facilitating their activation. FABP5 is overexpressed in PC, and correlates with poor patient prognosis and survival. Genetic knockdown or silencing of FABP5 decreases the proliferation and invasiveness of PC cells in vitro, and reduces tumor growth and metastasis in vivo. Pharmacological FABP5-specific inhibitors also reduce tumor growth and metastases, and produce synergistic effects with taxanes. In this review, we present current data supporting FABP5 as a novel molecular target for PC.