Recent studies have identified a unique role for high mobility group protein A1 (HMGA1) as a major regulator of tumor progression and in diverse tumor models. Emerging evidences indicate that overexpressed HMGA1 facilitates multiple malignant phenotypes of cancer cells, however, the oncogenic activities of HMGA1 in endometrial cancer (EC) remains elusive. Here we showed that HMGA1 was more frequently expressed in human EC tissues compared to non-tumor tissues. Elevated HMGA1 was significantly associated with advanced clinical stage. Wound-healing assay and transwell assay showed that HMGA1 can positively regulate cell migration and invasion. Mechanistically, luciferase reporter assay and Western blotting assay demonstrated that activation of Wnt/β-catenin pathway contributed to the oncogenic activity of HMGA1. Taken together, our data reveal that HMGA1 may function as an oncogene and modulate EC cell migration and invasion by activating Wnt/β-catenin pathway, implying that suppression of HMGA1 might be a potential therapeutic strategy for EC.