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.

新的证据表明，脂质信号传导失调是前列腺癌（PC）的一个关键因素，通过脂肪酸激活核受体过氧化物酶体增殖物激活受体（PPAR），导致促肿瘤基因上调。脂肪酸结合蛋白 (FABP) 是细胞内脂质结合蛋白，可将脂肪酸转运至 PPAR，促进其激活。 FABP5 在 PC 中过度表达，与患者不良预后和生存相关。 FABP5的基因敲低或沉默可降低体外PC细胞的增殖和侵袭性，并减少体内肿瘤的生长和转移。药理学 FABP5 特异性抑制剂还可减少肿瘤生长和转移，并与紫杉烷类药物产生协同作用。在这篇综述中，我们提供了支持 FABP5 作为 PC 新型分子靶点的最新数据。