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Background: Hyperglycemia or hyperinsulinemia contributes to poorer endometrial cancer survival. It was shown that P-LAP/IRAP translocates to the plasma membrane in response to insulin stimulation. Recently, we demonstrated that P-LAP/IRAP is associated with a poor prognosis in endometrial adenocarcinoma patients. The aim of this study was to examine whether the malignant potential of endometrial cancer enhanced by P-LAP/IRAP is due to increased glucose uptake via the P-LAP/IRAP-mediated activation of insulin signaling. Methods: We transfected P-LAP/IRAP cDNA into A-MEC cells (endometrial adenocarcinoma cell line), and A-MEC-LAP cells expressed a remarkably high level of GLUT4 proteins. Results: 3H-2-deoxyglucose uptake which responds to insulin in A-MEC-LAP cells was significantly higher than that of A-MEC-pc cells. A-MEC-LAP cells exhibited a significant growth-stimulatory effect compared to A-MEC-pc cells. A-MEC-LAP cells expressed a remarkably high level of p85PI3K protein compared to A-MEC-pc cells, and showed a higher degree of AKT phosphorylation by insulin stimulation. Conclusion: In summary, P-LAP/IRAP was involved in the increasing malignant potential of endometrial cancer mediated by insulin. P-LAP/IRAP was suggested to be a potential new target of molecular-targeted therapy for endometrial cancer. Background Endometrial carcinoma is the most common gynecological malignancy in the United States. Recently, the incidence of this disease has been increasing in Japan. Several personal and lifestyle-related characteristics, such as age, obesity, diabetes, and estrogen therapy, have been identified as risk factors for developing endometrial cancer [1]. A recent study showed that diabetes is associated with reduced survival after endometrial cancer, independent of tumor stage and grade [2]. This finding suggested the possibility of a diabetes-related condition, such as hyperglycemia or hyperinsulinemia, contributing to reduced survival in endometrial cancer patients. Furthermore, an in vitro study showed that endometrial cancer cells have high-affinity binding sites for insulin and proliferate in response to insulin exposure [3]. Several studies have Published: 19 January 2007 BMC Cancer 2007, 7:15 doi:10.1186/1471-2407-7-15 Received: 04 August 2006 Accepted: 19 January 2007 This article is available from: http://www.biomedcentral.com/1471-2407/7/15 © 2007 Shibata et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.