Accumulating evidence has proved that glioma stem-like cells (GSCs) are responsible for tumorigenesis, treatment resistance, and subsequent tumor recurrence in glioblastoma (GBM). In this study, we identified dual specificity protein kinase TTK (TTK) as the most up-regulated and differentially expressed kinase encoding genes in GSCs. Functionally, TTK was essential for in vitro clonogenicity and in vivo tumor propagation in GSCs. Clinically, TTK expression was highly enriched in GBM, moreover, was inversely correlated with a poor prognosis in GBM patients. Mechanistically, mitochondrial fission regulator 2 (MTFR2) was identified as one of the most correlated genes to TTK and transcriptionally regulated TTK expression via activation of TTK promoter. Collectively, MTFR2-dependent regulation of TTK plays a key role in maintaining GSCs in GBM and is a potential novel druggable target for GBM.

The VEGF - 634 CC and +936 TT genotypes were associated with a higher risk of glioma in a Han Chinese population.

Glioma is the most common primary malignancy of the central nervous system and is associated with high mortality rates. despite the available treatment options including surgery, radiotherapy and chemotherapy, the median patient survival rate is low. Therefore, the development of novel anticancer agents for the treatment of glioma is urgently required. Tanshinone I (TS I) is a tanshinone compound that is isolated from danshen. Accumulating evidence indicates that TS I exhibits antiproliferative activity in a variety of cancer types. However, the role of TS I and its mechanism of action in human glioma remain to be elucidated. In the present study, the anticancer potential of TS I against human glioma U87 MG cells was investigated. The results indicated that TS I exerted a potential cytotoxic effect on human glioma U87 MG cells. TS I was found to induce cell proliferation, inhibition, cell cycle arrest, apoptosis and autophagy in U87 MG cells. Mechanistic experiments indicated that TS I activated endoplasmic reticulum (ER) stress and inhibited AKT signaling and apoptosis in human glioma U87 MG cells. Furthermore, the present study demonstrated that TS I induced protective autophagy in U87 MG cells. Additionally, ER stress and AKT signal-mediated apoptosis and protective autophagy were found to be induced by TS I via intracellular reactive oxygen species accumulation. The results of the present study demonstrated that TS I may be a potential anticancer drug candidate that may be of value in the treatment of human glioma.

Glioma is the most common form of malignant primary brain tumor. WHO grading from 2016 classifies gliomas into four grades (I-IV) according to their histopathological signatures with astrocytomas, oligodendrogliomas, and mixed oligoastrocytomas being recognized as lower-grade gliomas (LGGs). 1,2 Importantly, the survival of LGG patients ranges widely when subgrouped by histological signature. The most frequent treatment approaches for LGGs are surgical resection combined with chemoradiotherapy. 3 However, tumor

Introduction:The insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme (ACE) gene has recently been linked to the pathogenesis and progression of human cancers. The aim of this study was to evaluate the potential association between ACE I/D polymorphism and glioma in a Chinese population. Materials and methods: A case-control study involving patients with 800 glioma and 800 controls was conducted. Polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) assay was applied to assess the ACE I/D genotypes. Results: Glioma cases had a significantly higher frequency of DD genotype [odds ratio (OR) = 1.61, 95% confidence interval (CI) = 1.12, 2.32; p = 0.01] than controls. When stratified by the grade of glioma, cases with WHO IV glioma had a significantly higher frequency of DD genotype (OR = 1.51, 95% CI = 1.03, 2.21; p = 0.03). When stratified by the histology of glioma, there was no significant difference in the distribution of each genotype. Conclusion: Our study suggested that the ACE DD genotype was associated with a higher glioma risk in this Chinese population. To the best of our knowledge, this is the first report describing the potential association between ACE I/D polymorphism and glioma. Additional studies are needed to confirm this finding.