Paeonol inhibits prostate cancer progression via the miR-145-5p/GOLM1 axis.

Paeonol, derived from Paeonia suffruticosa, is a potent ingredient known for its diverse benefits such as anti-tumor, antioxidant, and cardiovascular system protection. Currently, there is uncertainty about the impact of paeonol on prostate cancer (PCa). This research aims to explore how paeonol affects the PCa development and its specific mechanism. To screen the optimal concentration, the impact of paeonol on cell viability was examined via Cell Counting Kit-8 assay. The biological behaviors of PCa cells were evaluated via multiple approaches, including colony formation, Transwell, wound healing assay, and flow cytometry. MiR-145-5p level in PCa cells was assessed using quantitative real-time polymerase chain reaction (qRT-PCR), subsequently explored the impact of miR-145-5p overexpression on the biological properties of PCa cells. Bioinformatics analysis predicted the downstream target mRNA of miR-145-5p, while the dual-Luciferase reporter gene assay confirmed the targeting connection between the two. A subcutaneous xenograft tumor model was established to explore how paeonol may impact tumor growth by modulating miR-145-5p/Golgi membrane protein 1 (GOLM1). Results showed that Paeonol exerted suppressive effects on the malignant biological properties of PCa cells, along with induced apoptosis. PCa cells exhibited lower miR-145-5p level as opposed to normal cells, and paeonol treatment up-regulated miR-145-5p. GOLM1 was highly expressed in PCa cells, while miR-145-5p could directly target and downregulate GOLM1 expression. miR-145-5p overexpression suppressed the malignant biological properties of PCa cells, but GOLM1 overexpression reversed this effect. Silencing of miR-145-5p or GOLM1 overexpression both weakened the anti-tumor impacts of paeonol. Additionally, tumor growth was suppressed and apoptosis was induced in tumor cells in vivo by paeonol. In conclusion, Paeonol suppresses the malignant progression of PCa, and promotes cell apoptosis via regulating the miR-145-5p/GOLM1 axis.