SPOP enhances FADD degradation and decreases the activeness of the NF-κB signaling pathway in prostate cancer: an

Background: Speckle-type POZ protein (SPOP), FAS-associated protein with death domain (FADD), and nuclear transcription factor-κB (NF-κB) have been shown to be associated with the development of prostate cancer (PCa). FADD has been shown to activate the NF-κB pathway to promote tumorigenesis, while SPOP has been shown to enhance the breakdown of FADD and inhibit the function of the NF-κB signaling pathway in non-small cell lung cancer. The existence of this mechanism has not yet been confirmed in PCa. This study aimed to explore the mechanism by which SPOP regulates FADD and the NF-κB signaling pathway in PCa. Methods: Western blot was used to detect the presence of SPOP and FADD in both PCa cells and benign prostatic hyperplasia (BPH) cells. The biological behavior of the PC3 cells with altered levels of SPOP was examined using methods such as Cell Counting Kit 8, flow cytometry, and Transwell assay, and the effects of altering SPOP expression levels on the expression of FADD and NF-κB were assessed by western blot. The interaction between SPOP and FADD was detected by immunoprecipitation assay. The Results: The PCa cells displayed decreased Conclusions: There may be a SPOP-FADD-NF-κB regulatory axis in PCa. SPOP facilitates the degradation of FADD, leading to a decrease in the activity of the NF-κB signaling pathway.