There is increasing evidence that
coatomer protein complex subunit beta 2 (COPB2) plays an important role in various
cancer types. This study explored the role and the downstream mediators of COPB2 in
prostate cancer (PCa). The expression of COPB2 was determined by the
Cancer Genome Atlas database and
enzyme-linked
immunosorbent assay. COPB2 expression was upregulated in PCa tissues and correlated with Gleason score, biochemical recurrence, and poor prognosis. The functional roles of COPB2 in PCa were verified through a series of experiments. Knocking down COPB2 expression inhibited the growth and clonogenesis of PCa cells, promoted cell apoptosis, and inhibited the ability of scratch repair, invasion of PCa cells, and
tumor growth in Nude mice. To analyze downstream signaling pathways, ingenuity pathway analysis, GSEA, and whole-genome expression spectrum GeneChip analysis were used. Western blot revealed that COPB2 expression promoted the proliferation and invasion of PCa cells by regulating the MAPK/TGF-β signaling pathway. The interacting
protein (nuclear protein 1, NUPR1) was identified via Co-IP, real-time PCR, Western blot, and TCGA database in sampled tissues. The expressions of the interaction
proteins NUPR1 and COPB2 were negatively regulated by each other. COPB2 could be a new
biomarker for PCa diagnosis and monitoring and to provide a theoretical basis for identifying effective
drug intervention targets through in-depth mechanistic studies.