The Role of FADS2-Mediated FZD6 Regulation in Promoting Cell Proliferation and Apoptosis in Benign Prostatic Hyperplasia

With the aging population trend, benign prostatic hyperplasia (BPH) is prevalent in the middle-aged and elderly male demographic, characterized by a disruption in the balance of proliferation and apoptosis within the epithelial and stromal cells of the prostatic transition zone. This imbalance leads to a spectrum of complications, including lower urinary tract symptoms (LUTS). Fatty Acid Desaturase 2 (FADS2) has been linked to cell proliferation and apoptosis within the domain of oncology. Nonetheless, the precise role of FADS2 in BPH remains elusive. Our results reveal an elevation in FADS2 expression within BPH tissues, while knockdown of FADS2 curtails prostate cell proliferation and augments apoptosis. Moreover, the attenuation of FADS2 correlates with reduced expression of the Wnt signaling pathway receptor, FZD6. These findings accentuate the influence of FADS2 on the Wnt signaling cascade through the modulation of FZD6, thereby impacting the proliferation and apoptosis of prostate cells. Our investigation underscores the pivotal function of FADS2 in BPH and provides fresh perspectives on its control of prostate cell proliferation and apoptosis, underscoring the intricacies of FADS2's mechanisms in BPH.