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Introduction
Glioma, the most common form of brain malignancy, is one a major contributor to cancer-associated deaths worldwide (1). The strategies employed for the diagnosis and treatment of glioma have improved over the past several decades (2). However, the prognosis of patients with glioma remains poor, with a survival time of 12–18 months post-diagnosis (3). Therefore, the identification of the exact mechanisms underlying the malignant phenotype of glioma cells is required.
Neuroglobin (Ngb), a novel tumor-associated protein, functions as an oncogene or tumor suppressor in human cancer. Previous reports have demonstrated that overexpression of Ngb enhances reactive oxygen species scavenging and reverses oxidative stress-induced cell death in neuroblastoma cells (4–6). The expression of Ngb is upregulated under hypoxic conditions in glioblastoma cells and tumor xenografts, indicating a potential role of Ngb in cancer cell survival in hypoxic microenvironments (7,8). In addition to brain tumors, aberrant expression of Ngb has also been reported in other types of malignancies. For example, Ngb is reported to be overexpressed in certain non-small cell lung cancer cases, particularly in squamous cell carcinomas (9). Notably, 17β-estradiol induces Ngb upregulation, which renders cancer cells, including MCF-7, HepG2, SK-N-BE, HeLa and DLD-1, resistant to oxidative stress (10–13). However, Ngb expression is downregulated in hepatocellular carcinoma tissues and its silencing promotes the proliferation and cell cycle progression of cancer cells (14). Our previous study demonstrated that Ngb functions as an independent prognostic biomarker for patients with glioma and promotes the growth of cancer cells by suppressing apoptosis (15). However, the mechanisms underlying the survival-enhancing effect of Ngb in glioma remains a challenge, therefore, the present study aimed to investigate the effect and mechanisms of Ngb in glioma.
The results of the present study demonstrated that Ngb promoted the proliferation and inhibited the apoptosis of glioma cells, which may occur through effects on the phosphatidylinositol 3-kinase (PI3K)/AKT pathway. To the best of our knowledge, the presents study is the first to indicate that Ngb may be a potential therapeutic target for glioma.
Materials and methods
Cell culture and transfection
U87MG ATCC and U251MG human glioma cell lines were obtained from the American Type Culture Collection (Manassas, VA, USA) and were cultivated in Dulbecco's modified Eagle's medium (DMEM; Thermo Fisher Scientific, Inc., Waltham, MA, USA) supplemented...