Research Paper Volume 12, Issue 14 pp 14699—14717

Acetylation-mediated degradation of HSD17B4 regulates the progression of prostate cancer

Figure 8. K669 acetylation is downregulated in human PCa samples. (AB) Immunohistochemical staining of K669-acetylated and total HSD17B4 proteins in tumor and adjacent tissues. Examples are shown in (A), and the statistical analysis of all samples is shown in (B). Scale bars: 100 mm. The intensities of the K669-acetylated (left panel) and total (right panel) HSD17B4 protein were quantified, followed by statistical analysis. A total of 10 PCa tissues and 10 adjacent normal prostate tissues were analyzed. The mean value of multiple samples and the standard deviation are presented. (C) Working model. The increase in K669 acetylation promotes HSD17B4 degradation via CMA and then slows down the progression of PCa. CREBBP increases the HSD17B4 acetylation level and promotes its degradation, while SIRT3 can deacetylate K669 acetylation and stabilize its protein level. The accumulation of HSD17B4 can lead to consistent proliferation and migration of PCa cells. Data are shown as the mean ± SD (n = 3) or typical photographs of one representative experiment. Similar results were obtained in three independent experiments. *p < 0.05, **p < 0.01, ***p <0.001.