ABSTRACT
Lysine acetyltransferase 5 (KAT5), a member of the MYST family, can participate in cellular processes such as transcription, DNA repair, differentiation and signal transduction by acetylating different substrates. The role of KAT5 cannot be replaced by other MYST family members, and the knockout of KAT5 can directly lead to apoptosis, indicating that KAT5 may be located in the upstream of physiological signaling pathways in cells and play an extremely important and unique role. Therefore, the changes in KAT5 expression are very likely to lead to the occurrence and development of tumors. Previous studies have found that KAT5 is downregulated in breast cancer, melanoma, and lung cancer, and is considered a tumor suppressor in these tumors. However, in recent years, studies have found that KAT5 can be either highly or lowly expressed in breast cancer, liver cancer, melanoma, prostate cancer, lung cancer and other tumors. On the premise of high KAT5 expression, KAT5 can play a tumor-promoting role. While on the premise of low KAT5 expression, KAT5 can also play as a tumor suppressor. With further decrease of KAT5 expression, its tumor suppressive effect is weakened, which may lead to the occurrence and development of tumors. In addition, KAT5 has also been found to be differentially expressed in osteosarcoma, thyroid cancer, glioblastoma, colorectal cancer and other tumors, and the differential expression of KAT5 is closely related to the proliferation, metastasis, apoptosis, drug and radiotherapy resistance of tumor cells. Therefore, KAT5 is one of the potential tumor therapeutic targets. Here, we summarize the expression of KAT5 in tumors and the tumor-suppressing or tumor-promoting signaling pathways involved in the corresponding expression in recent years, hoping to provide new inspiration and reference for tumor treatment and prognosis monitoring.
ABSTRACT
Objective: To investigate the effects of lysine acetyltransferase (Kat5) on the proliferation and apoptosis of thyroid papillary carcinoma cells. Methods: RT-PCR and Western blotting methods were used to determine the expression levels of Kat5 mRNA and protein in the thyroid papillary carcinoma BHP10-3. TPC-1 . K1 cells and thyroid epithelial Nthy-ori3-l cells. The thyroid papillary carcinoma TPC-1 cells were divided into blank control group, negative control group and silencing Kat5 group (si-Kat5 group). The cells in blank control group were not transfected. the cells in negative control group were transfected with negative control siRNA. and the cells in si-Kat5 group were transfected with Kat5 siRNA. The expression levels of Kat5 mRNA and protein in the thyroid papillary carcinoma TPC-1 cells in various groups were detected by RT-PCR and Western blotting methods. The proliferation activities of the TPC-1 cells in various groups were measured by CCK-8 method, the colony formation assay was used to measure the clone formation rates of the TPC-1 cells in various groups, the apoptotic rates of the TPC-1 cells in various groups were detected by flow cytometry, and the expression levels of cyclin-dependent kinase 2 (CDK2). P21, P53. cleaved caspase-3. P13K, phosphorylated P13K (p-P13K), AKT, and phosphorylated AKT (p-AKT) protein in the TPC-1 cells in various groups were detected by Western blotting method. Results: The expression levels of Kat5 mRNA and protein in the thyroid papillary carcinoma BHP10-3. TPC-1 and K1 cells were higher than those in thyroid epithelial Nthy-ori3-l cells (P<0. 05). The differences in the Kat5 mRNA and protein expression levels, the proliferation activities, the clone formation rates, the apoptotic rates and the expression levels of CDK2. P21. P53. cleaved caspase-3. P13K. p-P13K . AKT and p-AKT proteins in the TPCM cells between various groups were statistically significant (P<0.05). Compared with blank control group and negative control group, the expression levels of Kat5 mRNA and protein in the TPC-1 cells in si-Kat5 group were decreased ( P