Histone acetyltransferase 1 promotes ovarian cancer progression by regulating cell proliferation and the cell cycle.

Ovarian cancer (OC) is the most common cause of gynecological cancer-related death. Histone acetyltransferase 1 (HAT1) has generated interest as a potential target for therapy due to it being involved in a variety of diseases, including cancer. However, to the best of our knowledge, the role of HAT1 in OC has not yet been investigated. In the present study, HAT1 was upregulated in OC and the high expression of HAT1 was associated with unfavorable prognosis. The transcription factor forkhead box protein A1 (FOXA1) transcriptionally regulated HAT1 expression. Furthermore, HAT1 knockdown in OC cells significantly suppressed cell proliferation and colony formation. In addition, the inhibition of HAT1 promoted cell cycle arrest, and reduced cyclin-dependent kinase (CDK)2, CDK4 and cyclin E levels in OC cells. Taken together, the present data suggested that HAT1 served an oncogenic role in OC; therefore, HAT1 may represents a new potential therapeutic target in OC treatment.