ACAT1 promotes bladder tumorigenesis by inducing cell cycle via AKT/GSK3ß/c-Myc signaling pathway
Acetyl-CoA acetyltransferase 1 (ACAT1) played a key role in regulating gene expression and tumorigenesis. Nevertheless, the biological function of ACAT1 in bladder cancer (BLCA) has yet to be elucidated. This study aimed to elucidate the bioinformatics features and biological functions of ACAT1 in BLCA. Here, we demonstrate for the first time that ACAT1 is elevated in BLCA tissues, correlating with specific clinicopathological features and an unfavorable prognosis for survival in BLCA patients. ACAT1 emerged as an independent risk factor in BLCA. Phenotypically, ACAT1 knockdown inhibited the proliferation and migration of BLCA cells both in vivo and in vitro, whereas ACAT1 overexpression yielded the opposite phenotype. Mechanistically, ACAT1 enhances BLCA cells proliferation by activating cell cycle through AKT/GSK3ß/c-Myc signaling pathway. In conclusion, this study identifies ACAT1 as an oncogene in BLCA, demonstrating its capability to promote proliferation and metastasis of BLCA. This suggests that ACAT1 may serve as a potential molecular target for the diagnosis and treatment of BLCA. Overall design: To investigate the role of ACAT1 in bladder cancer (BLCA), we first used two kinds of siRNA with different sequences, but both with excellent knockdown efficiency, to knock down the target gene ACAT1 in UM-UC-3 and T24 BLCA cell lines. Then, in order to ensure the reliability of the results, we performed independent experiments three times for each sample. Finally, the 18 samples were analyzed by RNA sequencing. (NC = negative control, Si1 = siACAT1-1, Si2 = siACAT1-2, UC3 = UM-UC-3)