KAT5 Negatively regulates the proliferation of prostate cancer LNCaP cells via the caspase 3-dependent apoptosis pathway.

Prostate cancer is one of the most common cancers in men over the age of sixty. Lysine acetyltransferase 5 (KAT5) is a histone acetyltransferase involved in transcriptional regulation, DNA repair, and cell signaling pathways. Previous studies have shown that KAT5 expression is reduced in the cytoplasm of the prostate cancer cell line LNCaP when exposed to androgen. Moreover, KAT5 has been reported to have a role in the molecular pathway leading to androgen-independent prostate cancer after long-term androgen deprivation therapy. Here, we showed that KAT5 expression was significantly reduced in prostate cancer tissues and cell lines by using the public databases Oncomine and Human Protein Atlas. Reduced KAT5 expression was significantly associated with high mortality in prostate cancer patients. Furthermore, KAT5 overexpression increased the level of apoptotic markers, such as cleaved-caspase 3, in LNCaP cells, thus enhancing the apoptotic death of LNCaP cells. Taken together, KAT5 induced apoptosis in prostate cancer cells via the caspase-3 pathway, indicating that KAT5 could be a gene therapy target for prostate cancer.