The high mobility group A2 (HMGA2), an oncofetal protein, was shown to play a role in tumor development and progression. However, the molecular and clinical role of HMGA2 in epithelial ovarian carcinomas (EOCs) is still unknown. In the present study, EOC cell line SKOV3 was subjected to in vitro assays. Here, our findings showed that HMGA2 was highly expressed in EOC cell line SKOV3. HMGA2 knockdown promoted cell apoptosis and the cleavage of caspase 3, and decreased the B cell lymphoma 2 (Bcl-2)/Bax ratio in SKOV3. Functionally, HMGA2 knockdown resulted in reduction of SKOV3 cell migration and invasion. Mechanically, HMGA2 knockdown affected the occurrence of EMT by increasing E-cadherin gene and protein expression and decreasing the gene and protein expression of N-cadherin, slug, and vimentin. At the same time, HMGA2 also repressed the expression of matrix metalloproteinase 2 (MMP2) and matrix metalloproteinase 9 (MMP9), which was consistent with the decreased invasion capacity. In conclusion, HMGA2 is associated with migration and invasiveness and regulates the progression of EMT in the development of EOC, and HMGA2 gene and protein may be a novel therapeutic target against EOC in the clinical practice.
Keywords: EMT; Epithelial ovarian carcinomas; HMGA2.