Anhui Provincial Stereotactic Neurosurgical Institute

Hefei, China

Anhui Provincial Stereotactic Neurosurgical Institute

Hefei, China
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Bao D.,Anhui Medical University | Bao D.,Anhui Provincial Stereotactic Neurosurgical Institute | Bao D.,Anhui Province Key Laboratory of Brain Function and Brain Disease | Cheng C.,Anhui Medical University | And 13 more authors.
Oncotarget | Year: 2017

The incidence of glioma in men is higher than that in women; however, little is known about the expression and basic function of the androgen receptor (AR) in gliomas. AR inhibited the small VCP/p97-interacting protein (SVIP) on the transcriptional level was previously reported. The present study shows that the protein level of AR is highly expressed in cell lines of the nervous system. Moreover, the AR expression is increased while SVIP expression is decreased in tumor tissue of glioma patients, which is in agreement with the progressing WHO grades. A statistically significant increase in serum testosterone level of glioma patients compared with that of non-cancer patients was also detected. Furthermore, it has been proved that SVIP is down-regulated as well as AR is up-regulated in glioma cell lines with R1881 treatment. Interestingly, the depletion of SVIP using siRNA facilitated cell proliferation and decreased p53 expression. In addition, overexpression of SVIP increased cell death only in p53wt cell lines. Moreover, U87MG cells, p53wt cell line was susceptible to AR antagonists in vitro and in vivo. The current study provides insight into the biological role of AR in suppressing SVIP and p53 and promoting the progression of glioma as well as the clinical treatment of glioma patients.


Mei J.,Anhui Medical University | Mei J.,Anhui Provincial Stereotactic Neurosurgical Institute | Niu C.,Anhui Medical University | Niu C.,Anhui Provincial Stereotactic Neurosurgical Institute
Neuroscience Letters | Year: 2010

The ubiquitin-proteasome system plays a central role in regulated degradation of cellular proteins under different physiological conditions. Accumulation of misfolded proteins is involved in the pathogenesis of many neurodegenerative diseases, such as Parkinson's disease (PD), Alzheimer's disease (AD) and Huntington's disease (HD). Hrd1 is a newly identified ubiquitin ligase involved in degradation of misfolded proteins from the endoplasmic reticulum (ER), thereby protecting cells against ER stress. Increasing evidence has linked ER stress to PD pathogenesis. However, the expression of Hrd1 in PD brain remains elusive. In the present study, the expression of Hrd1 in different encephalic regions was studied in 6-OHDA model of Parkinson's disease by immunohistochemistry. The results showed that Hrd1 was up-regulated in 6-OHDA-treated mice in various encephalic regional neurons, especially those in hippocampus, substantia nigra (SN), subthalamic nucleus (STN), striatum and frontal lobe. It suggested that Hrd1 up-regulation may represent a protective response against neurodegeneration in PD. © 2010 Elsevier Ireland Ltd.


Niu C.S.,Anhui Provincial Hospital | Niu C.S.,Anhui Province Key Laboratory of Brain Function and Brain Disease | Niu C.S.,Anhui Provincial Stereotactic Neurosurgical Institute | Yang Y.,Anhui Provincial Hospital | And 3 more authors.
International Journal of Oncology | Year: 2013

MiR-134 is a brain-enriched miRNA that plays an essential role in the development of the embryonic stem cell-orientated differentiation to central nervous system by suppression of Nanog and neural development (including neurons, cylindraxile and dendrites) and has been shown to be downregulated in oligodendrogliomas (ODG) and glioblastomas (GBM), suggesting its possible involvement in brain tumor progression. In this study, we defined the expression and function of miR-134, which we found to be downregulated in glioma samples and the glioblastoma cell line U87 by SYBR green real-time quantitative reverse transcription-PCR (real-time PCR). Early reports have characterized Nanog as a direct target of miR-134 by a dual-luciferase reporter assay in 293T cells. In our study, overexpression of miR-134 in U87 glioblastoma cells resulted in significant downregulation of Nanog mRNA levels as well as protein levels. miR-134 overexpression reduced the proliferation, invasiveness and migration capability of U87 cells while promoted apoptosis of these cells in vitro and suppressed the growth of tumor xenografts in vivo. These findings demonstrated that miR-134 deregulation is common in human gliomas. Restoration of its function inhibits cell proliferation, invasion and migration capability and promotes apoptosis, which could be partly due to its inhibitory effect on Nanog protein expression in glioblastoma cells. MiR-134 could play an important role as a tumor suppressor relying on its direct translational attenuation of Nanog.


Niu C.,Anhui Medical University | Zhang J.,Anhui Medical University | Zhang J.,Anhui Provincial Stereotactic Neurosurgical Institute | Mei J.,Anhui Medical University | Fu X.,Anhui Medical University
Medical Hypotheses | Year: 2011

Parkinson's disease (PD) is a common progressive neurodegenerative disorder whose core symptoms are tremor, bradykinesia, rigidity, and postural instability. Currently available treatment of PD is mainly based on dopamine replacement strategy to provide relief of motor symptoms, but cannot halt or reverse the degenerative processes of disease. Considerable in vitro and in vivo studies have found that neurotrophic factor (NTF) has neuroprotective or even neurorestorative properties on dopaminergic (DA) system, promoting them become promising candidates for the treatment of PD. However, the precise mechanism of NTF's effect in PD remains to be elucidated. Though the etiopathogenesis of PD has remained elusive, recently, compelling evidence has converged to suggest that failure of the ubiquitin-proteasome system (UPS) to degrade unwanted proteins may underlie nigralstrital degeneration and Lewy body (LB) formation which occurs in PD. In support of this, proteasome inhibitor has been successfully induced a PD modal both in vivo and in vitro. Many NTFs have been proved to posses definitely a therapy effect in a PD animal modal. Whether NTF can co-function with UPS that accomplishes the aim to protect and reserve dopaminergic neurons' function from neurotoxicity injury induced by proteasome inhibitor? If this hypothesis could be confirmed, it will represent a valuable advancement in the study of PD. Moreover, investigation of the functional link between UPS and NTF should also provide useful information for understanding the pathogenesis of PD. © 2011 Elsevier Ltd.


Gao G.,Anhui Medical University | Niu C.-S.,Anhui Provincial Stereotactic Neurosurgical Institute | Dong Y.-F.,Anhui Medical University | Zhang J.,Anhui Medical University | Ding W.-H.,Anhui Medical University
Journal of Clinical Rehabilitative Tissue Engineering Research | Year: 2010

BACKGROUND: PEX gene can interfere with the invasion acts of malignant glioma. Bone marrow mesenchymal stem cells (MSCs) are a new type of targeted cell vector on cancer therapy. OBJECTIVE: To construct MSCs stably expressing PEX gene. METHODS: PEX eukaryotic expression vector was constructed by molecular cloning, and identified the recombinant plasmid pcDNA3.1(+)-PEX by restriction endonuclease digestion and sequencing. After transfected with MSCs, the eukaryotic expression vector expression in MSCs was verified by immunocytochemical method. The MSCs stably expressing PEX was established by G418 selection, and then was detected by using reverse transcriptase-polymerase chain reaction. RESULTS AND CONCLUSION: The MSCs stably expressing PEX gene is successfully established, in which PEX gene is highly expressed at both gene level and protein level.


Niu C.S.,Anhui Medical University | Niu C.S.,Anhui Provincial Stereotactic Neurosurgical Institute | Li M.W.,Anhui Medical University | Ni Y.F.,Anhui Medical University | And 4 more authors.
Journal of Experimental and Clinical Cancer Research | Year: 2010

Objective. To investigate the effect of all-trans retinoic acid(ATRA) on the proliferation and differentiation of brain tumor stem cells(BTSCs) in vitro. Methods. Limiting dilution and clonogenic assay were used to isolate and screen BTSCs from the fresh specimen of human brain glioblastoma. The obtained BTSCs, which were cultured in serum-free medium, were classified into four groups in accordance with the composition of the different treatments. The proliferation of the BTSCs was evaluated by MTT assay. The BTSCs were induced to differentiate in serum-containing medium, and classified into the ATRA group and control group. On the 10th day of induction, the expressions of CD133 and glial fibrillary acidic protein (GFAP) in the differentiated BTSCs were detected by immunofluorescence. The differentiated BTSCs were cultured in serum-free medium, the percentage and the time required for formation of brain tumor spheres (BTS) were observed. Results. BTSCs obtained by limiting dilution were all identified as CD133-positive by immunofluorescence. In serum-free medium, the proliferation of BTSCs in the ATRA group was observed significantly faster than that in the control group, but slower than that in the growth factor group and ATRA/growth factor group, and the size of the BTS in the ATRA group was smaller than that in the latter two groups(P < 0.01). In serum-containing medium, the expression percentages of CD133 and GFAP in the differentiated BTSCs were (2.29% ± 0.27%) and (75.60% ± 4.03%) respectively in the ATRA group, and (7.05% ± 0.49%) and (12.51% ± 0.77%) respectively in the control group. The differentiation rate of BTSCs in the ATRA group was significantly higher than that in the control group (P < 0.05), but there was still CD133 expressed in the ATRA group. The differentiated BTSCs could re-form BTSs in serum-free medium. The percentage of BTS formation in the ATRA group was(4.84% ± 0.32%), significantly lower than that in the control group (17.71% ± 0.78%) (P < 0.05), and the time required for BTS formation in the ATRA group was (10.07 ± 1.03)d, significantly longer than that in the control group (4.08 ± 0.35)d (P < 0.05). Conclusion. ATRA can promote the proliferation and induce the differentiation of BTSCs, but the differentiation is incomplete, terminal differentiation cannot be achieved and BTSs can be formed again. © 2010 Niu et al; licensee BioMed Central Ltd.


He H.,Anhui Medical University | Li M.W.,Anhui Medical University | Niu C.S.,Anhui Medical University | Niu C.S.,Anhui Provincial Stereotactic Neurosurgical Institute
Journal of Clinical Neuroscience | Year: 2012

Brain tumor stem cells (BTSC) are predicted to be critical drivers of tumor progression due to their self-renewal capacity and limitless proliferative potential. Recent studies suggest that stem cells are controlled by a particular microenvironment known as a "niche". We therefore analysed human glioma tissues and found that the CD133 + and nestin + niches are perivascularly localized in all glioma tissues. Furthermore, there is a positive correlation between the CD133 + niches and CD133 + blood vessels, which is similar to the correlation between the nestin + niches and nestin + blood vessels. We demonstrate that both CD133 + blood vessels and nestin + blood vessels have an important role in maintaining the structure of the glioma stem cell niche. Moreover, the abundance of CD133 + niches and nestin + niches increases significantly as tumor grade increases. These findings provide a new insight into the biology of BTSC and open a new perspective for targeted therapy against the brain tumors. © 2011 Elsevier Ltd. All rights reserved.


Yang Y.,Anhui Medical University | Yang Y.,Anhui Province Key Laboratory of Brain Function and Brain Disease | Niu C.-S.,Anhui Medical University | Niu C.-S.,Anhui Province Key Laboratory of Brain Function and Brain Disease | And 3 more authors.
Oncology Reports | Year: 2013

The stemness gene Nanog has been shown to play an important role in tumor development, including glioma. Nanog is phosphorylated at multiple Ser/Thr-Pro motifs, which promotes the interaction between Nanog and the prolyl isomerase Pin1, leading to Nanog stabilization by suppressing its ubiquitination. The present study investigated the expres sion and relationship of Pin1 and Nanog in human gliomas. Significantly higher mRNA and protein expression levels of Pin1 and Nanog were demonstrated in 120 glioma specimens of different pathological grades by RT-PCR, immunohis tochemistry staining and western blot analysis. The relative levels of Pin1 expression, as well as Nanog expression, were significantly positively correlated with pathological grade. Moreover, a positive correlation of Pin1 and Nanog expres sion in human gliomas was noted. Co-localization of Pin1 and Nanog was observed in the perinuclear space in the cytoplasm of glioma cells detected by immunofluorescence staining. Significantly positive correlation between Pin1 and Nanog in gliomas indicated that Pin1 and Nanog may be related to tumorigenesis and development of glioma cells.


Niu C.-S.,Anhui Medical University | Niu C.-S.,Anhui Provincial Stereotactic Neurosurgical Institute | Li D.-X.,Anhui Medical University | Li D.-X.,Anhui Provincial Stereotactic Neurosurgical Institute | And 6 more authors.
Oncology Reports | Year: 2011

Stemness genes, including NANOG, which have been reported to play a significant role in embryonic stem cells (ESCs), are purported to be expressed in specific human tumor types. In the present study, we explored the expression of NANOG in gliomas to demonstrate its key roles in maintaining the undifferentiated state of glioma cells. Brain tumor stem cells (BTSCs) were isolated from the human glioma cell line U87 and cultured in simplified serum-free medium. Significantly higher NANOG mRNA and protein expression levels were demonstrated in U87 parental attached cells and suspended BTSCs as well as in 69 glioma specimens of different pathological grades. The relative levels of NANOG mRNA and protein expression were higher in the BTSCs as compared to those in the U87 parental attached cells and were significantly positively correlated with pathological grade. The coexpression and relationship of NANOG, CD133 and GFAP in situ in the cellular levels was determined through double-label immunohistochemical staining in the gliomas. A positive correlation of NANOG and CD133 expression with pathological grade of the samples was noted, while NANOG and GFAP expression correlated negatively with the pathological grade (P<0.01). Overexpression of NANOG in gliomas and its close relationship with the undifferentiated state of glioma cells in vivo and in vitro indicated that NANOG may contribute to the existence of BTSCs and may be related to tumorigenesis of the cerebrum by maintaining the undifferentiated state of glioma cells, which provides a foundation to further explore its role in the biological behavior of gliomas.


He H.U.,Anhui Medical University | Chao Niu S.H.I.,Anhui Medical University | Chao Niu S.H.I.,Anhui Provincial Stereotactic Neurosurgical Institute | Ming W.U.L.I.,Anhui Medical University
Oncology Reports | Year: 2012

Glioblastoma multiforme (GBM) is the most lethal type of brain tumor. The formation of abnormal, dysfunctional tumor vasculature and glioblastoma stem-like cells (GSCs) are believed to be the major components of the inability to treat these tumors effectively. We analyzed 70 glioblastoma samples by immunohistochemistry and double immunofluorescence staining. The immunohistochemical expression of the putative brain tumor stem cell markers CD133 and Nestin in paraffin sections was analyzed using morphometry. In all GBM samples, CD133 or Nestin was expressed in tumor and endothelial cells. Double immunofluorescence stainings showed that the two different marked GSCs were found accumulated around the CD31 + blood vessels and CD133/CD31 or Nestin/CD31 co-expression was found in the endothelial cells and GSCs. Furthermore, the vascular endothelial growth factor (VEGF) and the endothelial marker CD31 were co-expressed in GSCs. Therefore, GSCs not only showed distinct perivascular distribution but were capable of differentiating into endothelial cells. We demonstrate that GSCs contribute directly to the tumor vasculature by endothelial cell differentiation. GSCs and tumor vascularization are closely related to each other, not only in the regional distribution but also in biological function. These findings describe a new mechanism for tumor vasculogenesis and may provide new insights for targeted therapy against brain tumors.

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