Abstract

The success of using glycolytic inhibitors for cancer treatment relies on better understanding the roles of each frequently deregulated glycolytic genes in cancer. This report analyzed the involvement of a key glycolytic enzyme, alpha-enolase (ENO1), in tumor progression and prognosis of human glioma. ENO1 expression levels were examined in glioma tissues and normal brain (NB) tissues. The molecular mechanisms of ENO1 expression and its effects on cell growth, migration and invasion were also explored by 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT) assay, Transwell chamber assay, Boyden chamber assay, Western blot and in vivo tumorigenesis in nude mice. ENO1 mRNA and protein levels were upregulated in glioma tissues compared to NB. In addition, increased ENO1 was associated disease progression in glioma samples. Knocking down ENO1 expression not only significantly decreased cell proliferation, but also markedly inhibited cell migration and invasion as well as in vivo tumorigenesis. Mechanistic analyses revealed that Cyclin D1, Cyclin E1, pRb, and NF-κB were downregulated after stable ENO1 knockdown in glioma U251 and U87 cells. Conversely, knockdown of ENO1 resulted in restoration of E-cadherin expression and suppression of mesenchymal cell markers, such as Vimentin, Snail, N-Cadherin, β-Catenin and Slug. Furthermore, ENO1 suppression inactivated PI3K/Akt pathway regulating the cell growth and epithelial-mesenchymal transition (EMT) progression. Overexpression of ENO1 is associated with glioma progression. Knockdown of ENO1 expression led to suppressed cell growth, migration and invasion progression by inactivating the PI3K/Akt pathway in glioma cells.

Highlights

  • Correction After the publication of this work [1] it was brought to the authors’ attention that the U251-pLVTHM panel in Figure fiveB and the U251 negative control (NC) panel in Figure fiveD contained a duplication in error

  • The authors regret any inconvenience that this inaccuracy may have caused

  • Research which is freely available for redistribution

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Summary

Introduction

Correction After the publication of this work [1] it was brought to the authors’ attention that the U251-pLVTHM panel in Figure fiveB and the U251 negative control (NC) panel in Figure fiveD contained a duplication in error. Correction: Alpha-enolase as a potential cancer prognostic marker promotes cell growth, migration, and invasion in glioma Ye Song1,2†, Qisheng Luo1,3†, Hao Long1†, Zheng Hu1, Tianshi Que1, Xi’an Zhang1, Zhiyong Li1, Gang Wang1, Liu Yi1, Zhen Liu2,4*, WeiYi Fang2* and Songtao Qi1*

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