• Title, Summary, Keyword: Glioma

Search Result 348, Processing Time 0.047 seconds

Induction of Apoptosis in Glioma Cells and Upregulation of Fas Expression Using the Human Interferon-β Gene

  • Guo, Yan;Wang, Gan;Gao, Wen-Wei;Cheng, Shi-Wen;Wang, Ren;Ju, Shi-Ming;Cao, He-Li;Tian, Heng-Li
    • Asian Pacific Journal of Cancer Prevention
    • /
    • v.13 no.6
    • /
    • pp.2837-2840
    • /
    • 2012
  • We investigated whether IFN-${\beta}$ inhibits the growth of human malignant glioma and induces glioma cell apoptosis using the human IFN-${\beta}$ gene transfected into glioma cells. A eukaryonic expression vector ($pSV2IFN{\beta}$) for IFN-${\beta}$ was transfected into the glioma cell line SHG44 using liposome transfection. Stable transfection and IFN-${\beta}$ expression were confirmed using an enzyme-linked immunosorbent assay (ELISA). Cell apoptosis was also assessed by Hoechst staining and electron microscopy. In vivo experiments were used to establish a SHG44 glioma model in nude mice. Liposomes containing the human IFN-${\beta}$ gene were injected into the SHG44 glioma of nude mice to observe glioma growth and calculate tumor size. Fas expression was evaluated using immunohistochemistry. The IFN-${\beta}$ gene was successfully transfected and expressed in the SHG44 glioma cells in vitro. A significant difference in the number of apoptotic cells was observed between transfected and non-transfected cells. Glioma growth in nude mice was inhibited in vivo, with significant induction of apoptosis. Fas expression was also elevated. The IFN-${\beta}$ gene induces apoptosis in glioma cells, possibly through upregulation of Fas. The IFN-${\beta}$ gene modulation in the Fas pathway and apoptosis in glioma cells may be important for the treatment of gliomas.

Association Between Genetic Polymorphism of XRCC1 Gene and Risk of Glioma in а Chinese Population

  • Wang, Ying-Xin;Fan, Kai;Tao, Ding-Bo;Dong, Xiang
    • Asian Pacific Journal of Cancer Prevention
    • /
    • v.14 no.10
    • /
    • pp.5957-5960
    • /
    • 2013
  • Background: Gliomas are the most common type of primary brain tumor in adults, and the X-ray repair complementing group 1 gene (XRCC1) is an important candidate gene influencing its risk. The objective of this study was to detect the influence of XRCC1 genetic polymorphisms on glioma risk. Materials and Methods: A total of 629 glioma patients and 641 cancer-free subjects were enrolled in this case-control study. The genotypes of the c.1471G>A genetic polymorphism were determined by created restriction site-polymerase chain reaction (CRS-PCR) and DNA sequencing methods. The influence of the XRCC1 genetic polymorphism on glioma risk was evaluated by association analysis. Results: Our data indicated that the alleles/genotype of this genetic variant was statistically associated with glioma risk. The AA genotype was statistically associated with the increased risk of glioma compared to the GG wild genotype (odds ratios (OR) = 1.89, 95% CI 1.25-2.87, P = 0.003). The allele-A may contribute to increased the susceptibility to glioma (OR = 1.23, 95% CI 1.04-1.46, P = 0.017). Conclusions: These preliminary findings indicate that the c.1471G>A genetic polymorphism of XRCC1 has the potential to influence glioma susceptibility, and might be used as molecular marker for assessing glioma risk.

Elevated Serum IL-17A but not IL-6 in Glioma Versus Meningioma and Schwannoma

  • Doroudchi, Mehrnoosh;Pishe, Zahra Ghanaat;Malekzadeh, Mahyar;Golmoghaddam, Hossein;Taghipour, Mousa;Ghaderi, Abbas
    • Asian Pacific Journal of Cancer Prevention
    • /
    • v.14 no.9
    • /
    • pp.5225-5230
    • /
    • 2013
  • Background: There is a Th1/Th2 cytokine imbalance and expression of IL-17 in patients with brain tumours. We aimed to compare the levels of IL-17A and IL-6 in sera of glioma, meningioma and schwannoma patients as well as in healthy individuals. Materials and Methods: IL-17A and IL-6 levels were measured in sera of 38 glioma, 24 meningioma and 18 schwannoma patients for comparison with 26 healthy controls by commercial ELISA assays. Results: We observed an increase in the IL-17A in 30% of glioma patients while only 4% and 5.5% of meningioma and schwannoma patients and none of the healthy controls showed elevated IL-17A in their sera ($0.29{\pm}0.54$, $0.03{\pm}0.15$ and $0.16{\pm}0.68$ vs. $0.00{\pm}0.00pg/ml$; p=0.01, p=0.01 and p=0.001, respectively). There was also a significant decrease in the level of IL-6 in glioma patients compared to healthy controls ($2.34{\pm}4.35$ vs. $4.67{\pm}4.32pg/ml$; p=0.01). There was a direct correlation between the level of IL-17A and age in glioma patients (p=0.005). Glioma patients over 30 years of age had higher IL-17A and lower IL-6 in their sera compared to the young patients. In addition, a non-significant grade-specific inverse trend between IL-17A and IL-6 was observed in glioma patients, where high-grade gliomas had higher IL-17A and lower IL-6. Conclusions: Our data suggest a Th17 mediated inflammatory response in the pathogenesis of glioma. Moreover, tuning of IL-6 and IL-17A inflammatory cytokines occurs during progression of glioma. IL-17A may be a potential biomarker and/or immunotherapeutic target in glioma cases.

FoxD2-AS1 is a prognostic factor in glioma and promotes temozolomide resistance in a O6-methylguanine-DNA methyltransferase-dependent manner

  • Shangguan, Wenbing;Lv, Xuyang;Tian, Nan
    • The Korean Journal of Physiology and Pharmacology
    • /
    • v.23 no.6
    • /
    • pp.475-482
    • /
    • 2019
  • Glioma is the most common brain tumor with a dismal prognosis. While temozolomide (TMZ) based chemotherapy significantly improves survival in glioma patients, resistance against this compound commonly leads to glioma treatment failure. Overexpression of long-noncoding RNA (LncRNA) FoxD2 adjacent opposite strand RNA 1 (FoxD2-AS1) was identified to promote glioma development, but the role in TMZ resistance remains unclear. In this paper, we found that FoxD2-AS1 was overexpressed in recurrent glioma, high FoxD2-AS1 expression was significantly correlated with poor patient outcome. Methylation of $O^6$-methylguanine-DNA methyltransferase (MGMT) is significantly less frequent in high FoxD2-AS1 expression patients. Knockdown of FoxD2-AS1 decreased the proliferation, metastatic ability of glioma cells and promote the sensitivity to TMZ in glioma cells. Furthermore, knockdown of FoxD2-AS1 induced hypermethylation of the promoter region of MGMT. Our data suggested that FoxD2-AS1 is a clinical relevance LncRNA and mediates TMZ resistance by regulating the methylation status of the MGMT promoter region.

Inhibitory Effects of Toxoplasma Antigen on Proliferation and Invasion of Human Glioma Cells

  • Choo, Juk-Dong;Lee, Jong-Soo;Kang, Jong-Sul;Lee, Hyun-Sung;Yeom, Jin-Young;Lee, Young-Ha
    • Journal of Korean Neurosurgical Society
    • /
    • v.37 no.2
    • /
    • pp.129-136
    • /
    • 2005
  • Objective: Currently available therapies for human malignant gliomas have limited efficacy. Toxoplasma gondii, an obligate intracellular protozoan parasite, and Quil-A are nonspecific, potent immune stimulants. T. gondii is shown to have antitumor activity in some types of cancers. Therefore, this study is undertaken to evaluate the antitumor effect of Toxoplasma lysate antigen (TLA), alone or in combination with Quil-A, on human glioma U373MG and U87MG cells. Methods: The in vitro effects of TLA alone or in combination with Quil-A on the proliferation, invasion, and apoptosis of glioma cells were tested using MTT, Matrigel invasion, and DNA fragmentation assays, and the in vivo effects on the growth of gliomas were evaluated in athymic nude mice transplanted with glioma cells. Results: Treatment with TLA resulted in the suppressed proliferation and invasion of both U373MG and U87MG cells, in a dose-dependent manner. In addition, at high concentration, TLA induced glioma cell apoptosis. When TLA was administered in the mouse glioma model, malignant glioma growth was decreased. The combined treatment of TLA with Quil-A significantly inhibited the proliferation and invasion of cultured cells as well as tumor mass of implanted mice. Conclusion: TLA inhibits the proliferation and invasion of glioma cells in vitro and in vivo, and these antitumor effects of TLA are significantly enhanced by the addition of Quil-A.

Xeroderma Pigmentosum Complementation Group F Polymorphisms Influence Risk of Glioma

  • Cheng, Hong-Bin;Xie, Chen;Zhang, Ru-You;Hu, Shao-Shan;Wang, Zhi;Yue, Wu
    • Asian Pacific Journal of Cancer Prevention
    • /
    • v.14 no.7
    • /
    • pp.4083-4087
    • /
    • 2013
  • We conducted an exploratory investigation of whether variation in six common SNPs of xeroderma pigmentosum complementation group F (XPF) is associated with risk of glioma in a Chinese population. Six single nucleotide polymorphisms (SNPs) were genotyped in 207 glioma cases and 236 cancer-free controls by a 384-well plate format on the Sequenom MassARRAY platform (Sequenom, San Diego, USA). The rs1800067 G and rs2276466 G allele frequencies were significantly higher in the glioma group than controls. Individuals with the rs1800067 GG genotype were at greater risk of glioma when compared with the A/A genotype in the codominant model, with an OR (95% CI) of 2.63 (1.04-7.25). The rs2276466 polymorphism was significantly associated with moderate increased risk of glioma in codominant and dominant models, with ORs (95% CI) of 1.90 (1.05-3.44) and 1.55 (1.07-2.47), respectively. The combination genotype of rs1800067 G and rs2276466 G alleles was associated with a reduced risk of glioma (OR=0.44, 95% CI=0.19-0.98). These findings indicate that genetic variants of the XPF gene have critical functions in the development of glioma.

Glioma-Associated Oncogene Homolog1 (Gli1)-Aquaporin1 pathway promotes glioma cell metastasis

  • Liao, Zheng-qiang;Ye, Ming;Yu, Pei-gen;Xiao, Chun;Lin, Feng-yun
    • BMB Reports
    • /
    • v.49 no.7
    • /
    • pp.394-399
    • /
    • 2016
  • Glioma-Associated Oncogene Homolog1 (Gli1) is known to be activated in malignant glioma; however, its downstream pathway has not been fully explained. The aim of this study was to explore the role of Gli1-Aquaporin1 (AQP1) signal pathway in glioma cell survival. Our data suggests that both Gli1 and AQP1 are upregulated in glioma tissues, as in comparison to in normal tissues. These up-regulation phenomena were also observed in glioma U251 and U87 cells. It was demonstrated that Gli1 positively regulated the AQP1 expression. By luciferase reporter gene and ChIP assay, we observed that this modulation process was realized by combination of Gli1 with AQP1 promotor. In addition, knock down of Gli1 by siRNA interference reduced the viability of glioma cells as well as suppressed cell metastasis. Also, the inhibitory effects of cell survival by silenced Gli1 were abrogated by AQP1 overexpression. In summary, glioma cell survival is a regulatory process and can be mediated by Gli1-AQP1 pathway.

Lgr4 Promotes Glioma Cell Proliferation through Activation of Wnt Signaling

  • Yu, Chun-Yong;Liang, Guo-Biao;Du, Peng;Liu, Yun-Hui
    • Asian Pacific Journal of Cancer Prevention
    • /
    • v.14 no.8
    • /
    • pp.4907-4911
    • /
    • 2013
  • The key signaling networks regulating glioma cell proliferation remain poorly defined. The leucine-rich repeat containing G-protein coupled receptor 4 (Lgr4) has been implicated in intestinal, gastric, and epidermal cell functions. We investigated whether Lgr4 functions in glioma cells and found that Lgr4 expression was significantly increased in glioma tissues. In addition, Lgr4 overexpression promoted while its knockdown using small interfering RNA oligos inhibited glioma cell proliferation. In addition, Wnt/${\beta}$-catenin signaling was activated in cells overexpressing Lgr4. Therefore, our results revealed that Lgr4 activates Wnt/${\beta}$-catenin signaling to regulate glioma cell proliferation.

Chordoid Glioma : an Uncommon Tumor of the Third Ventricle

  • Park, Seong-Hyun;Hwang, Jeong-Hyun
    • Journal of Korean Neurosurgical Society
    • /
    • v.40 no.1
    • /
    • pp.40-43
    • /
    • 2006
  • Chordoid glioma is an uncommon low-grade tumor of the third ventricle with histologic features of a chordoma and immunolabeling for glial fibrillary acid protein. We present a rare case of a patient with a chordoid glioma of the third ventricle and review the literature regarding this tumor's clinical, radiological and pathologic aspects.

Microglial Contribution to Glioma Progression: an Immunohistochemical Study in Eastern India

  • Ghosh, Krishnendu;Ghosh, Samarendranath;Chatterjee, Uttara;Chaudhuri, Swapna;Ghosh, Anirban
    • Asian Pacific Journal of Cancer Prevention
    • /
    • v.17 no.6
    • /
    • pp.2767-2773
    • /
    • 2016
  • Human glioma, arising from glial cells of the central nervous system, accounts for almost 30%of all brain tumours, neoplasms with a poor prognosis and high mortality rates worldwide. In the present study we assessed tissue architectural modifications associated with macrophage lineage cells, controversial major immune effector cells within the brain, in human glioma tissue samples from eastern India. Ethically cleared post-operative human glioma samples from our collaborative neurosurgery unit with respective CT/MRI and patient history were collected from the Nodal Centre of Neurosciences in Kolkata, over 9 months. Along with conventional histopathology, samples were subjected to silver-gold staining and fluorescence tagged immunophenotyping for the detection of electron dense brain macrophage/microglia cells in glioma tissue, followed by immune-phenotyping of cells. With higher grades, CD11b+/Iba-1+ macrophage/microglia architecture with de-structured boundaries of glioma lesions indicated malfunction and invasive effector state. Present study documented a contribution of microglia to glioma progression in Eastern India.