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Xiao G.,The Institute of Skull Base Surgery and Neurooncology at Hunan | Tang Z.,Central South University | Yuan X.,The Institute of Skull Base Surgery and Neurooncology at Hunan | Yuan J.,The Institute of Skull Base Surgery and Neurooncology at Hunan | And 4 more authors.
Oncology Letters | Year: 2015

Wnt-1 inducible signaling pathway protein-2 (WISP-2) is a member of the CCN family, which is critical for the control of cell morphology, motion, adhesion and other processes involved in tumorigenesis. The expression pattern and clinical significance of WISP-2 in astrocytomas remains unclear. In this study, reverse transcription-polymerase chain reaction was performed to systematically investigate the expression of WISP-2 in 47 astrocytoma tissues of different pathological grades and 10 normal brain tissues. The mRNA expression levels of WISP-2 in the astrocytoma tissues were observed to be significantly higher than those in the normal brain tissues. Furthermore, the upregulation of WISP-2 was found to be associated with astrocytomas of higher pathological grades. Subsequently, 154 astrocytoma and 15 normal brain tissues were analyzed using immunohistochemistry and similar results were obtained. Univariate and multivariate survival analyses were used to determine the correlations between WISP-2 expression and overall survival (OS) and progression-free survival (PFS). The results indicated that the expression of WISP-2 was found to negatively correlate with patient PFS and OS. These results demonstrated that the WISP-2 protein is involved in the pathogenesis and progression of human astrocytomas and may serve as a malignant biomarker of this disease. © 2015, Spandidos Publications. All rights reserved. Source


Li X.,Central South University | Li X.,The Institute of Skull Base Surgery and Neurooncology at Hunan | Liu F.,Central South University | Liu F.,The Institute of Skull Base Surgery and Neurooncology at Hunan | And 8 more authors.
International Journal of Biological Macromolecules | Year: 2014

In recent years there has been an increasing interest in naturally occurring substances in plant origin that may be used as potential chemopreventive and chemotherapeutic agents to prevent or slow the progression of chronic illnesses, such as cancer. In this study, we aimed at examining the antitumor activity of Atractylodes macrocephala polysaccharide (AMPs) in vitro using glioma C6 cells and the underlying mechanisms were also investigated. The results demonstrated that AMPs significantly inhibited proliferation of C6 cells in a concentration dependent manner by DNA fragmentation and apoptosis induction. Besides, AMPs treatment induced the loss of mitochondrial membrane potential and caused release of cytochrome c to cytosol. Furthermore, the activation of capase-3, caspase-9 and poly(ADP-ribose) polymerase (PARP) cleavage occurred following AMPs treatment in C6 cells. These results suggested that the induction of apoptosis via the mitochondrial pathway was involved in the anti-proliferative activity of AMPs against glioma C6 cells. © 2014 Elsevier B.V. Source


Huang C.,JiShou University | Yuan X.,Central South University | Yuan X.,The Institute of Skull Base Surgery and Neurooncology at Hunan | Li Z.,Central South University | And 6 more authors.
International Journal of Clinical and Experimental Pathology | Year: 2014

This study investigated the role of VE-statin/Egfl7 and its mechanism in angiogenesis in malignant glioma. Transwell culture plates were used to establish an U251-HUVEC co-culture system, which was used to mimic the interaction between malignant glioma and endothelial cells. Lentiviral vectors expressing VE-statin/Egfl7 siRNA were constructed, and U251 cells and HUVECs were transfected to inhibit VE-statin/Egfl7 expression. The proliferation, adherence, migration, and lumen formation of endothelial cells were assayed to investigate the influence of VE-statin/Egfl7 on angiogenesis in malignant glioma in vitro. Data showed that HUVEC growth was temporarily slowed after silencing the VE-statin/Egfl7 gene but rapidly returned to normal. Although endothelial cell migration was not influenced, cell adherence was markedly inhibited. Furthermore, the endothelial cells failed to generate a capillary-like lumen after VE-statin/Egfl7 gene silencing. Therefore, it can be concluded that VE-statin/Egfl7 may regulate the adherence of endothelial cells, thus playing an important role in endothelium-induced lumen formation during angiogenesis in malignant glioma. Source


Huang C.,JiShou University | Yuan X.,Central South University | Yuan X.,The Institute of Skull Base Surgery and Neurooncology at Hunan | Wan Y.,JiShou University | And 7 more authors.
International Journal of Clinical and Experimental Pathology | Year: 2014

This study investigated VE-statin/Egfl7 expression and its role and regulatory mechanism in malignant glioma progression. Forty-five paraffin-embedded glioma (grade I-II: n=24; grade III-IV: n=21) were examined. VE-statin/Egfl7 protein expression was detected via immunohistochemistry, and its correlation with pathological grade was evaluated. Three-dimensional cell culture was then performed to investigate the influence of VE-statin/Egfl7 on the angiogenesis of umbilical vein endothelial cells. Microarray detection was used to molecularly profile VE-statin/Egfl7 and relevant signaling pathways in malignant glioma (U251 cells). Data showed that VE-statin/Egfl7 protein was mainly expressed in the cytoplasm of cancer and vascular endothelial cells and was significantly related to the degree of malignancy (t=4.399, P<0.01). Additionally, VE-statin/Egfl7 expression was low in certain gray-matter neurons but undetectable in glial cells. VE-statin/Egfl7 gene silencing significantly inhibited angiogenesis in umbilical vein endothelial cells. The following microarray results were observed in VE-statin/Egfl7-silenced U251 cells: 1) EGFR family members showed the highest differential expression, accounting for 5.54% of differentially expressed genes; 2) cell survival-related signaling pathways changed significantly; and 3) the integrin αγβ3 signaling pathway was markedly altered. Thus, malignant glioma cells and glioma vascular endothelial cells highly express VE-statin/Egfl7, which is significantly correlated with the degree of malignancy. Moreover, VE-statin/Egfl7 plays an important role in glioma angiogenesis. Microarray results indicate that VE-statin/Egfl7 may regulate EGFR and integrins to influence the FAK activity of downstream factors, triggering the PI3K/Akt and Ras/MAPK cascades and subsequent malignant glioma development. Source

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