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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. Source

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. Source

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. Source

Niu C.S.,CAS Hefei Institutes of Physical Science | Niu C.S.,Anhui Province Key Laboratory of Brain Function and Brain Disease | Niu C.S.,Anhui Provincial Stereotactic Neurosurgical Institute | Yang Y.,CAS Hefei Institutes of Physical Science | 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. Source

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. Source

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