Endometrial cancer (EC) is the most common gynecological cancer and is clinically classified as Type I or Type II. Type I EC expresses the estrogen receptor ERα, while Type II EC does not and is associated with a poorer prognosis. However, it was found that both Type I (RL95-2) and Type II (KLE) EC cells respond to estrogen, suggesting that an alternative receptor may be responsible for estrogen signaling in Type II EC. Previous studies have shown that G- protein-coupled receptor-30 (GPR30) can also modulate physiological responses to estrogen. GPR30 has also been implicated in epithelial-mesenchymal transition (EMT), which facilitates metastasis by inducing changes in cell characteristics. In this study, it was confirmed that KLE cells responded to estrogen and expressed GPR30. Inhibition of GPR30 in KLE cells decreased cell migration and viability. Furthermore, KLE cells expressed increased levels of vimentin and Snail compared to RL95-2 cells, which are associated with a mesenchymal phenotype. To demonstrate a direct connection between GPR30 and EMT, RL95-2 cells were treated with TGFβ to induce EMT, and levels of GPR30 increased. Understanding the role of GPR30 in Type II EC could lead to expanded therapy options, particularly for patients at risk for metastatic disease.