The deregulation of histone deacetylase 1 (HDAC1) is reportedly involved in the progression of several cancer types. However, its function in endometrial cancer remains unknown. The aim of the present study was to clarify the role of HDAC1 in aerobic glycolysis and the progression of endometrial cancer. Lentiviral vector transfection was used to up- and downregulate HDAC1 expression in HEC-1-A endometrial cancer cells. The effects of HDAC1 on cellular proliferation, apoptosis, migration, invasiveness and tumorigenesis were determined by CCK-8, flow cytometry, wound-healing, transwell chamber and in vivo tumor formation experiments, respectively. HDAC1 level was significantly increased in endometrial cancer tissues and cells, and its high expression was associated with advanced clinicopathological progression. HEC-1-A cell proliferation, invasiveness, migration and tumorigenesis were enhanced, and apoptosis was inhibited when HDAC1 was overexpressed. Moreover, upregulation of HDAC1 significantly promoted the epithelial-mesenchymal transition of HEC-1-A cells, and increased glucose consumption, lactate secretion and ATP levels. Collectively, the present study revealed that HDAC1 promoted the aerobic glycolysis and progression of endometrial cancer, which may provide a potential target for endometrial cancer treatment.
Keywords: aerobic glycolysis; epithelial-mesenchymal transition; growth; histone deacetylase 1; migration.
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