Fdps, also known as Farnesyl diphosphate synthase, is an enzyme in the mevalonate pathway. It plays a crucial role in the synthesis of farnesyl diphosphate, which is essential for the prenylation of small GTPases and is involved in multiple cellular signaling pathways, with significant importance in cell growth, proliferation, and differentiation [1].

In PTEN-deficient prostate cancer (PCa), Fdps overexpression synergizes with PTEN deficiency in PTEN conditionally knockout mice. Ectopic overexpression of Fdps promotes oncogenic phenotypes like colony formation and proliferation through activation of AKT and ERK signaling by prenylating Rho A, Rho G, and CDC42 small GTPases. Conversely, knockdown of Fdps in PCa cells reduces colony growth and proliferation by modulating AKT and ERK pathways. Pharmacological targeting of Fdps by zoledronic acid also decreases the growth and clonogenicity of human and murine PCa cells and 3D tumoroids by disrupting AKT and ERK signaling [1].

In glioma, a remarkable enhancement in Fdps level was observed in tissues, contributing to tumour growth and macrophage infiltration. Fdps activated the Wnt/β-catenin signalling pathway and ultimately facilitated macrophage infiltration by inducing CCL20 expression [2].

In conclusion, Fdps is an important enzyme in the mevalonate pathway, playing a significant role in cancer-related processes. Studies using PTEN-deficient and sufficient mouse models in PCa and in glioma tissues have revealed that Fdps promotes cancer cell growth, proliferation, and macrophage infiltration in these malignancies. These findings suggest that Fdps could potentially be a therapeutic target for treating prostate cancer and glioma.