共查询到20条相似文献,搜索用时 31 毫秒
1.
TLR9 expression in glioma tissues correlated to glioma progression and the prognosis of GBM patients
Background
Our study aims to evaluate the expression of TLR9 in glioma tissues, examine the association between TLR9 expression, clinicopathological variables, and glioma patient outcome, we further characterized the direct effects of TLR9 agonist CpG ODN upon the proliferation and invasion of glioma cells in vitro. 相似文献2.
Toyoda A Yokota A Saito T Kawana H Higashi M Suzuki Y Tanaka T Kitagawa M Harigaya K 《International journal of oncology》2011,38(1):89-96
The human ortholog of mammalian enabled (hMena), a member of the enabled/vasodilator-stimulated phosphoprotein (Ena/VASP) family, is an actin regulatory protein involved in the regulation of cell motility. Increasing evidence suggests that hMena overexpression is involved in human cancers, but the upstream events that influence the expression of hMena remain to be elucidated. In this study, we performed immunohistochemical analysis of the expression of hMena protein in paraffin-embedded archival tissues of infiltrating ductal carcinomas (IDCs) obtained from 52 cases. We found that elevated hMena expression is associated with larger tumor size (>2.5 cm, p<0.01), HER2 expression (p<0.05), p53 index (p<0.03) and Ki67 index (p<0.01), suggesting that hMena is a predictor of poor prognosis in IDCs. The histological characteristics of each specimen showed that hMena was overexpressed in the tumor cells at the invasive front of IDCs, indicating that hMena expression is at least partly mediated by tumor cell-matrix interactions. To explore the role of the absence of p53 function in hMena overexpression of IDCs, wild-type p53 cDNA was introduced into SW620 cells, which originally express mutant p53. In wild-type p53-transfected cells, hMena mRNA expression was decreased to 70% of the levels in mock transfected cells (p<0.01). In conclusion, our study indicates that hMena overexpression is involved in the progression of IDCs, and raises the possibility that wild-type p53 may suppress hMena expression. 相似文献
3.
Clemens Seidel Nils Dörner Matthias Osswald Antje Wick Michael Platten Martin Bendszus Wolfgang Wick 《BMC cancer》2011,11(1):127
Background
Peritumoral edema is a characteristic feature of malignant glioma related to the extent of neovascularisation and to vascular endothelial growth factor (VEGF) expression. 相似文献4.
背景与目的:有研究表明hMena可通过EGF启动细胞内多条信号传导道路,指导细胞迁移、黏附、增殖、分化、凋亡等过程。本研究探讨EGF通过上调hMena的表达对胶质瘤细胞迁移运动能力的影响。方法:Western blot检测经100ng/mLEGF处理的人胶质瘤细胞系LN229细胞hMena的表达情况,观察细胞形态的变化,划痕实验与Transwell检测细胞迁移运动能力。结果:100ng/mL EGF可上调人胶质瘤细胞系LN229细胞中hMena的表达(P<0.05),经EGF处理后LN229细胞伪足明显增多,穿过transwell小孔的细胞数为73.67±6.57,显著高于对照组(38.00±5.51)(P<0.05),划痕损伤后迁移的距离为(106.71±5.49)μm,显著高于对照组细胞迁移距离(69.67±6.12)μm,(P<0.05)。结论:EGF可以上调hMena的表达,并增强细胞的迁移运动能力。 相似文献
5.
Gerald N DeLorenze Lucie McCoy Ai-Lin Tsai Charles P QuesenberryJr Terri Rice Dora Il'yasova Margaret Wrensch 《BMC cancer》2010,10(1):215
Background
Malignant glioma is a rare cancer with poor survival. The influence of diet and antioxidant intake on glioma survival is not well understood. The current study examines the association between antioxidant intake and survival after glioma diagnosis. 相似文献6.
Maria S Pino Michele Balsamo Francesca Di Modugno Marcella Mottolese Massimo Alessio Elisa Melucci Michele Milella David J McConkey Ulrike Philippar Frank B Gertler Pier Giorgio Natali Paola Nisticò 《Clinical cancer research》2008,14(15):4943-4950
PURPOSE: hMena, member of the enabled/vasodilator-stimulated phosphoprotein family, is a cytoskeletal protein that is involved in the regulation of cell motility and adhesion. The aim of this study was to determine whether or not the expression of hMena isoforms correlated with sensitivity to EGFR tyrosine kinase inhibitors and could serve as markers with potential clinical use. EXPERIMENTAL DESIGN: Human pancreatic ductal adenocarcinoma cell lines were characterized for in vitro sensitivity to erlotinib, expression of HER family receptors, markers of epithelial to mesenchymal transition, and expression of hMena and its isoform hMena(+11a). The effects of epidermal growth factor (EGF) and erlotinib on hMena expression as well as the effect of hMena knockdown on cell proliferation were also evaluated. RESULTS: hMena was detected in all of the pancreatic tumor cell lines tested as well as in the majority of the human tumor samples [primary (92%) and metastatic (86%)]. Intriguingly, in vitro hMena(+11a) isoform was specifically associated with an epithelial phenotype, EGFR dependency, and sensitivity to erlotinib. In epithelial BxPC3 cells, epidermal growth factor up-regulated hMena/hMena(+11a) and erlotinib down-regulated expression. hMena knockdown reduced cell proliferation and mitogen-activated protein kinase and AKT activation in BxPC3 cells, and promoted the growth inhibitory effects of erlotinib. CONCLUSIONS: Collectively, our data indicate that the hMena(+11a) isoform is associated with an epithelial phenotype and identifies EGFR-dependent cell lines that are sensitive to the EGFR inhibitor erlotinib. The availability of anti-hMena(+11a)-specific probes may offer a new tool in pancreatic cancer management if these results can be verified prospectively in cancer patients. 相似文献
7.
Background
We previously identified brain type fatty acid-binding protein (FABP7) as a prognostic marker for patients with glioblastoma (GBM). Increased expression of FABP7 is associated with reduced survival. To investigate possible molecular mechanisms underlying this association, we compared the expression and subcellular localization of FABP7 in non-tumor brain tissues with different types of glioma, and examined the expression of FABP7 and epidermal growth factor receptor (EGFR) in GBM tumors. 相似文献8.
Jing Xiong Li Zhou Miao Yang Yoon Lim Yu-hong Zhu Deng-li Fu Zhi-wei Li Jin-hua Zhong Zhi-cheng Xiao Xin-Fu Zhou 《Neuro-oncology》2013,15(8):990-1007
Background
High-grade glioma is incurable, with a short survival time and poor prognosis. The increased expression of p75 neurotrophin receptor (NTR) is a characteristic of high-grade glioma, but the potential significance of increased p75NTR in this tumor is not fully understood. Since p75NTR is the receptor for the precursor of brain-derived neurotrophic factor (proBDNF), it is suggested that proBDNF may have an impact on glioma.Methods
In this study we investigated the expression of proBDNF and its receptors p75NTR and sortilin in 52 cases of human glioma and 13 cases of controls by immunochemistry, quantitative real-time PCR, and Western blot methods. Using C6 glioma cells as a model, we investigated the roles of proBDNF on C6 glioma cell differentiation, growth, apoptosis, and migration in vitro.Results
We found that the expression levels of proBDNF, p75NTR, and sortilin were significantly increased in high-grade glioma and were positively correlated with the malignancy of the tumor. We also observed that tumors expressed proBDNF, p75NTR, and sortilin in the same cells with different subcellular distributions, suggesting an autocrine or paracrine loop. The ratio of proBDNF to mature BDNF was decreased in high-grade glioma tissues and was negatively correlated with tumor grade. Using C6 glioma cells as a model, we found that proBDNF increased apoptosis and differentiation and decreased cell growth and migration in vitro via p75NTR.Conclusions
Our data indicate that proBDNF and its receptors are upregulated in high-grade glioma and might play an inhibitory effect on glioma. 相似文献9.
Kuan-Min Fang Chung-Shi Yang Tzu-Chien Lin Ti-Chun Chan Shun-Fen Tzeng 《Neuro-oncology》2014,16(4):552-566
Background
Glioma development is a multistep process associated with progressive genetic alterations but also regulated by cellular and noncellular components in a tumor-associated niche.Methods
Using 2 rat C6 glioma cell clones with different tumorigenesis, named C6-1 and C6-2, this study characterized genes associated with enhanced tumorigenic features of glioma cells by comparative cDNA microarray analysis combined with Q-PCR. Neurospehere formation and clonogenicity were examined to determine the growth of tumorigenic C6 glioma cells. The lentivirus-mediated gene knockdown approach was conducted to determine the role of interleukin-33 (IL-33) in glioma cell proliferation and migration. Transwell cell invasion assay was used to examine microglia migration induced by tumorigenic C6 cells.Results
The functional analysis of gene ontology (GO) biological processes shows that the upregulated genes found in tumorigenic C6 (C6-1) cells are closely related to cell proliferation. Tumorigenic C6 cells expressed cytokines and chemokines abundantly. Among these genes, IL-33 was profoundly induced in tumorigenic C6 cells with the expression of IL-33 receptor ST2. Furthermore, the growth rate and colony formation of tumorigenic C6 cells were attenuated by the inhibition of IL-33 and ST2 gene expression. Moreover, IL-33 was involved in tumorigenic glioma cell migration and regulation of the expression of several glioma-associated growth factors and chemokines in tumorigenic C6 cells.Conclusion
Accordingly, we concluded that glioma cells with abundant production of IL-33 grow rapidly; moreover, the interactions of multiple cytokines/chemokines induced by glioma cells may develop a microenvironment that facilitates microglia/macrophage infiltration and fosters glioma growth in the brain. 相似文献10.
11.
Shi-ming He Zhen-wei Zhao Yuan Wang Ji-pei Zhao Liang Wang Fang Hou Guo-dong Gao 《Journal of experimental & clinical cancer research : CR》2011,30(1):70
Background
To examine the expression of SMAD4 at gene and protein levels in glioma samples with different WHO grades and its association with survival.Methods
Two hundreds fifty-two glioma specimens and 42 normal control tissues were collected. Immunochemistry assay, quantitative real-time PCR and Western blot analysis were carried out to investigate the expression of SMAD4. Kaplan-Meier method and Cox''s proportional hazards model were used in survival analysis.Results
Immunohistochemistry showed that SMAD4 expression was decreased in glioma. SMAD4 mRNA and protein levels were both lower in glioma compared to control on real-time PCR and Western blot analysis (both P < 0.001). In addition, its expression levels decrease from grade I to grade IV glioma according to the results of real-time PCR, immunohistochemistry analysis and Western blot. Moreover, the survival rate of SMAD4-positive patients was higher than that of SMAD4-negative patients. We further confirmed that the loss of SMAD4 was a significant and independent prognostic indicator in glioma by multivariate analysis.Conclusions
Our data provides convincing evidence for the first time that the reduced expression of SMAD4 at gene and protein levels is correlated with poor outcome in patients with glioma. SMAD4 may play an inhibitive role during the development of glioma and may be a potential prognosis predictor of glioma. 相似文献12.
Marta Terrile Irene Appolloni Filippo Calzolari Roberto Perris Evelina Tutucci Paolo Malatesta 《BMC cancer》2010,10(1):550
Background
In the last years, the transmembrane proteoglycan NG2 has gained interest as a therapeutic target for the treatment of diverse tumor types, including gliomas, because increases of its expression correlate with dismal prognosis. NG2 has been shown to function as a co-receptor for PDGF ligands whose aberrant expression is common in gliomas. We have recently generated a glioma model based on the overexpression of PDGF-B in neural progenitors and here we investigated the possible relevance of NG2 during PDGF-driven gliomagenesis. 相似文献13.
Cheng-Chia Lee Chun-Lung Chou Ching-Jen Chen Huai-Che Yang Hsiu-Mei Wu Cheng-Ying Shiau David Hung-Chi Pan Wen-Yuh Chung 《Journal of neuro-oncology》2018,139(3):547-562
Purpose
MicroRNAs (miRNAs) have been shown to be involved in the initiation and progression of glioma. However, the underlying molecular mechanisms are still unclear.Methods
We performed microarray analysis to evaluate miRNA expression levels in 158 glioma tissue samples, and examined miR-1231 levels in glioma samples and healthy brain tissues using qRT-PCR. In vitro analyses were performed using miR-1231 mimics, inhibitors, and siRNA targeting EGFR. We used flow cytometry, CCK-8 assays, and colony formation assays to examine glioma proliferation and cell cycle analysis. A dual luciferase reporter assay was performed to examine miR-1231 regulation of EGFR, and the effect of upregulated miR-1231 was investigated in a subcutaneous GBM model.Results
We found that miR-1231 expression was decreased in human glioma tissues and negatively correlated with EGFR levels. Moreover, the downregulation of miR-1231 negatively correlated with the clinical stage of human glioma patients. miR-1231 overexpression dramatically downregulated glioma cell proliferation, and suppressed tumor growth in a nude mouse model. Bioinformatics prediction and a luciferase assay confirmed EGFR as a direct target of miR-1231. EGFR overexpression abrogated the suppressive effect of miR-1231 on the PI3K/AKT pathway and G1 arrest.Conclusions
Taken together, these results demonstrated that EGFR is a direct target of miR-1231. Our findings suggest that the miR-1231/EGFR axis may be a helpful future diagnostic target for malignant glioma.14.
15.
16.
Jian Zou Kun Wang Lei Han An-ling Zhang Zhen-dong Shi Pei-yu Pu Chun-sheng Kang 《临床肿瘤与癌症研究(英文版)》2011,8(3):144-148
Objective
To confirm the role played by AKT1 and AKT2 in the β-catenin/ Tcf-4 signaling pathway in promoting malignant transformation of glioma cells. 相似文献17.
Objective
Although causal relationships between smoking and cancer risk have been established for many sites, most studies of brain cancer have not supported an association. However, two recent cohort studies showed increased risks of glioma among smokers. We quantified the association between smoking and glioma through a meta-analysis of the literature. 相似文献18.
Karrie Mei-Yee Kiang Xiao-Qin Zhang Grace Pingde Zhang Ning Li Stephen Yin Cheng Ming-Wai Poon Jenny Kan-Suen Pu Wai-Man Lui Gilberto Ka-Kit Leung 《Targeted oncology》2017,12(3):353-363
Background
The long non-coding RNA CRNDE has emerged as an important regulator in carcinogenesis and cancer progression. While CRNDE has previously been found to be the most highly upregulated lncRNA in glioma, detailed information on its roles in regulating cancer cell growth remains limited.Objective
In the present study, we aimed at exploring the functional roles and underlying mechanisms of CRNDE in glioma.Methods
We applied microarray data analysis to determine the prognostic significance of CRNDE in glioma patients and its correlation with epidermal growth factor receptor (EGFR) activation. EGFR inhibition was used to confirm the role of EGFR in regulating CRNDE expression. Functional studies were performed upon CRNDE silencing to explore its role in gliomagenesis.Results
We confirm that CRNDE acts as an oncogene that is highly up-regulated in glioma, and high CRNDE expression correlates with poor prognosis in glioma patients. We further demonstrate that the expression of CRNDE correlates with EGFR activation. EGF and EGFR tyrosine kinase inhibitor (TKI) enhance and block the up-regulation of CRNDE expression, respectively, suggesting that EGFR signaling may positively regulate CRNDE expression. Functional assays show that CRNDE depletion inhibits glioma cell growth both in vitro and in vivo, and is associated with induced cellular apoptosis with decreased Bcl2/Bax ratio.Conclusions
Our findings suggest that the aberrant expression of CRNDE may be mediated by activated EGFR signaling and play significant roles in gliomagenesis.
19.
Sabit Delic Nadine Lottmann Anja Stelzl Franziska Liesenberg Marietta Wolter Silke G?tze Marc Zapatka Yuzuru Shiio Michael C. Sabel J?rg Felsberg Guido Reifenberger Markus J. Riemenschneider 《Neuro-oncology》2014,16(2):179-190