Abstract:Objective This study aims to explore the effect of palmitic acid (PA)-rich diet on prostate cancer (PCa) in mice.Method The TCGA database and immunohistochemistry (IHC) were used to analyze the differential expression of fatty acid synthase (FASN) between the PCa tissue and adjacent normal tissue. In addition, twelve nude mice were subcutaneously implanted with LNCaP cells and assigned into two groups. One group was fed a PA-rich diet, while the other group was fed a normal control (NC) diet. Twelve mice overexpressing the C-myc gene (C-mycT) were assigned into two groups and fed the same diets as the nude mice. The growth of PCa was analyzed by tumor mass measurement, HE staining, and Ki67 staining. Furthermore, the expression of epithelial-mesenchymal transition (EMT)-related proteins, such as E-cadherin, N-cadherin, and transforming growth factor (TGF)-β1, was determined by IHC and Western blot. Finally, relevant gene data were retrieved from the TCGA database and analyzed to explore the relationship among CD36, TGF-β1, and PCa.Result The expression of FASN was markedly higher in the PCa tissue than in the adjacent normal tissue, and there was a positive correlation between FASN expression and the progression of PCa. In nude mice and C-mycT mice, a PA-rich diet significantly promoted the progression of PCa, induced the EMT process, and activated the TGF-β1 signal. The expression of TGF-β1 was significantly associated with the decreased survival rate of individuals diagnosed with PCa. The expression of CD36 was positively correlated with TGF-β1. Highly expressed TGF-β1, TGF-βR1, and CD36 were risk factors for PCa, and TGF-β1 was an independent risk factor for PCa.Conclusion The PA-rich diet promoted the tumor growth, activated the TGF-β1 signal pathway, and induced EMT in the mouse model of PCa.
