ENO1 Inhibits Apoptosis and Promotes Cell Invasion and Proliferation in Malignant Melanoma

Abstract

Introduction The glycolytic enzyme, α-Enolase (ENO1), catalyzes the production of phosphoenolpyruvate from 2-phosphoglycerate, which enhances glycolysis, and thus contributes to tumor progression. In the present study, we aimed to determine ENO1’s role in malignant melanoma (MM) and the potential underlying mechanism. Methods Western blotting was used to assess the levels of ENO1, c-Myc, β-catenin, MMP-9, PGAM1, and MMP-13 in MM-derived cell lines or tumor tissues from patients with MM. Plasmids pCMV-SPORT6-ENO1 and pET-28a-ENO1siRNA plasmids were used to overexpress and knockdown ENO1 in MM cells, respectively. To determine the function of ENO1 in the malignant behavior of MM cells, we performed wound healing, Cell counting kit 8, Transwell chamber, and flow cytometry analyses. Pyruvate determination and lactic acid kits were used to evaluate the production of pyruvate and lactic acid in tumor cells. Results The protein levels of ENO1 and PGAM1 in MM tissue were significantly higher than that in mole tissue. In MM cells, ENO1 overexpression inhibited apoptosis; promoted invasion, migration, and proliferation; increased pyruvate and lactate production; and increased in β-catenin, MMP-9, MMP-13, and c-Myc levels. The opposite effects were observed in MM cells silenced for ENO1. Conclusion These results indicated that ENO1 is involved in MM progression by enhancing invasion and proliferation, while inhibiting apoptosis. In addition, ENO1 might have an important function in tumor cell glycolysis. Therefore, ENO1 represents a potential therapeutic target to treat MM.