1. Academic Validation
  2. Enolase-phosphatase 1 as a novel potential malignant glioma indicator promotes cell proliferation and migration

Enolase-phosphatase 1 as a novel potential malignant glioma indicator promotes cell proliferation and migration

  • Oncol Rep. 2018 Oct;40(4):2233-2241. doi: 10.3892/or.2018.6592.
Li Su 1 Ke Yang 2 Shun Li 1 Chen Liu 1 Jianguo Han 3 Yuan Zhang 2 Guozheng Xu 1
Affiliations

Affiliations

  • 1 Department of Neurosurgery, Wuhan General Hospital of PLA, Southern Medical University, Wuhan, Hubei 430070, P.R. China.
  • 2 The Central Laboratory, The First Affiliated Hospital of Shenzhen University, Shenzhen Second People's Hospital, Shenzhen, Guangdong 518035, P.R. China.
  • 3 Department of Neurosurgery, Shenzhen University General Hospital, Shenzhen, Guangdong 518055, P.R. China.
Abstract

Enolase-phosphatase 1 (ENOPH1), is an Enzyme that is involved in polyamine biosynthesis and is associated with stress responses. However, little is known about its role in the pathophysiology of glioma. In the present study, we examined the expression and function of ENOPH1 in human glioma tissues and cell lines. Western blot, qPCR and immunohistochemistry analysis were performed to investigate the expression of the ENOPH1 protein in glioma tissues in 86 patients. The 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT), wound healing and cell cycle assays were implemented to identify cell growth and cell migration in U87 and U251 glioma cells. The results revealed that compared with normal brain tissues, the level of ENOPH1 was markedly increased in glioma tissues. In addition, we observed that the glioma pathological grade was positively associated with the expression level of ENOPH1. Knockdown of ENOPH1 expression with siRNA markedly reduced cell proliferation, and significantly decreased cell migration. Notably, knockdown of ENOPH1 promoted its downstream protein, aci-reductone dioxygenase 1 (ADI1), to shift from the nucleus to the cytoplasm of U251 glioma cells, while MT1-MMP expression was significantly downregulated compared with the control group. Collectively, our data demonstrated that the knockdown of ENOPH1 suppressed cell growth and migration, which may be associated with ADI1 translocation and MT1-MMP downregulation in glioma cells. Thus, ENOPH1 could serve as an underlying therapeutic target of glioma.

Figures
Products