Abstract
ENO1 plays a paradoxical role in driving the pathogenesis of tumors. However, the clinical significance of ENO1 expression remains unclear and its function and modulatory mechanisms have never been reported in endometrial carcinoma (EC). In this study, ENO1 silencing significantly reduced cell glycolysis, proliferation, migration, and invasion in vitro, as well as tumorigenesis and metastasis in vivo by modulating p85 suppression. This in turn mediated inactivation of PI3K/AKT signaling and its downstream signals including glycolysis, cell cycle progression, and epithelial-mesenchymal transition (EMT)-associated genes. These effects on glycolysis and cell growth were not observed after ENO1 suppression in normal human endometrial epithelial cells (HEEC). Knocking down ENO1 could significantly enhance the sensitivity of EC cells to cisplatin (DDP) and markedly inhibited the growth of EC xenografts in vivo. In clinical samples, EC tissues exhibited higher expression levels of ENO1 mRNA and protein compared with normal endometrium tissues. Patients with higher ENO1 expression had a markedly shorter overall survival than patients with low ENO1 expression. We conclude that ENO1 favors carcinogenesis, representing a potential target for gene-based therapy.
Highlights
Endometrial Carcinoma (EC) is the most common gynecological malignancy and the fourth most common malignancy in women in the developed world today [1]
In order to further validate the role of ENO1 and its molecular basis in endometrial carcinoma (EC), we evaluated the expression of ENO1 in human normal endometrium (NE) and EC tissues, as well as its effects on cell glycolysis, growth, migration, and invasion in vitro as well as tumorigenicity and metastasis in vivo
Transcriptional levels of ENO1 were assessed by RT-PCR, with efficient knockdowns from shENO1-A in HEC-1B cell line and shENO1-C in Ishikawa cell line compared to the empty vector controls [pLVTHM-GFPControl (PLVTHM)] (P < 0.05) (Supplementary Figure 1B)
Summary
Endometrial Carcinoma (EC) is the most common gynecological malignancy and the fourth most common malignancy in women in the developed world today [1]. Further elucidation of the molecular mechanisms during endometrial cancer is urgently required
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