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Th Chang et al.'s report supporting an oncogenic role for ENO1 in NSCLC [13], but Camptothecin not Chang's study [15].In order to evaluate the function of ENO1 and eliminate the influence of MBP-1 on NSCLC, we firstly performed an immunofluorescence and observed that ENO1 was expressed in the cytoplasm but not in the nucleus (MBP-1) in A549 and SPCA-1 cells. Furthermore, we also found that MBP-1 was not expressed by Western blot assay in A549 and SPCA-1 cells. The abovementioned results suggested that both two cells could be used as welldefined models to evaluate the function of ENO1 on NSCLC. Further, stable ENO1-overexpressed A549 cells and stable ENO1-suppressed SPCA-1 cells as well as transient ENO1-suppressed A549 and SPCA-1 cells were respectively constructed, which was used to investigate the role of ENO1 in NSCLC. ENO1 was originally described as an enzyme responsible for the glycolytic pathway. To further assess the effect of ENO1 on NSCLC cells, we analyzed the glycolysis changes triggered by ENO1 and found that overexpressed and suppressed ENO1 respectively increased and decreased the production of lactate. These data suggested that ENO1 was involved in inducing glycolysis in NSCLC. Previous studies have demonstrated that ENO1 overexpression was positively associated with progression and poor prognosis in neuroendocrine tumors, neuroblastoma, pancreatic cancer, prostate cancer, cholangiocarcinoma, thyroid carcinoma, hepatocellular carcinoma, and breast cancer [14,21-27]. Further, ENO1 has been shown to promote cell proliferation, cycle progression, migration, and invasion [14,21-33], which suggests that ENO1 functions as an oncogene in tumor pathogenesis. In this study, we found that overexpressed ENO1 significantly elevated cell proliferation and clone formation in vitro as well as tumorigenesis in vivo. Furthermore, we also observed that overexpressed ENO1 induced cell migration, invasion, and metastasis in NSCLC. Our results are consistent with previous reports in other tumors that ENO1 functions as an oncogene [13,14,29,34] but are in contrast with Zhou et al.'s report that ENO1 overexpression suppressed EMT in NSCLC A549 cell line [16]. The biological functions of ENO1 found in this study provide a mechanistic basis for the pathological and clinical observations. When we examined the key regulators of the glycolysis and cell cycle at the G1-S phase transition, we discovered that suppression of ENO1 inhibitedFu et al. Journal of Hematology Oncology (2015)8:Page 7 ofFigure 4 ENO1 promotes cell migration and invasion. (A) Stably upregulated ENO1 elevated the migration and invasion of A549 cells in vitro. (B) Transiently knocking down ENO1 reduced the migration and invasion of A549 cells in vitro. (C, D) Stable and transient downregulated ENO1 reduced the migration and invasion of SPCA-1 cells in vitro. (E) External optical fluorescence images of liver were obtained 40 days after spleen injection. Representative photographs of H E staining of metastatic cancer tissues (M) are shown. Data are presented as mean ?SD for three independent experiments (*P PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/17139194 cycle and EMT-associated genes via FAK/PI3K/AKT pathway in NSCLC cells. (A) In A549 cells, overexpressed ENO1 increased the levels of p-Rb (ser 780) and oncogenic cell cycle regulators cyclin D1, cyclin E1, and c-Myc and decreased the expression of tumor suppressor p21. Conver.

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