Alpha-enolase as a potential cancer prognostic marker promotes cell growth, migration, and invasion in glioma

Abstract

BackgroundThe 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.MethodsENO1 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.ResultsENO1 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.ConclusionOverexpression 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.

ENO1 promotes tumor proliferation and cell adhesion mediated drug resistance (CAM-DR) in Non-Hodgkin's Lymphomas

“…4A). It has been reported that ENO1 can control the expression of cell cycle associated genes via PI3K/AKT pathway in glioma [12]. Therefore, we evaluated the expression of Cyclin D1 and Cyclin E in OCI-Ly8 and Daudi cells.…”

“…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 [12].…”

Diabetic Retinopathy and Laser Therapy in Rats: A Protein-Protein Interaction Network Analysis

“…63 It is shown that the knockdown of ENO1 expression led to suppressed cell growth and migration by inactivating the PI3K/Akt pathway in glioma cells. 63 Tear proteomic analysis of patients with type 2 diabetes with dry eye syndrome shows alteration in expression of ENO1 65 as well as results on DR in rat. 25 Another hub-bottleneck after laser therapy is ALDOA, which can be suggested as a common hub-bottleneck for DR progression and laser therapy.…”

“…Its overexpression has been associated with multiple tumors. [62][63][64] In many of these tumors, ENO1 promoted tumorgenesis via activating and regulating the PI3K/ AKT signaling pathway. 63 It is shown that the knockdown of ENO1 expression led to suppressed cell growth and migration by inactivating the PI3K/Akt pathway in glioma cells.…”

“…[62][63][64] In many of these tumors, ENO1 promoted tumorgenesis via activating and regulating the PI3K/ AKT signaling pathway. 63 It is shown that the knockdown of ENO1 expression led to suppressed cell growth and migration by inactivating the PI3K/Akt pathway in glioma cells. 63 Tear proteomic analysis of patients with type 2 diabetes with dry eye syndrome shows alteration in expression of ENO1 65 as well as results on DR in rat.…”