Ting Lei

Tongji Hospital, Wu-han-shih, Hubei, China

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Publications (88)140.72 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Surgery performed during the asymptomatic phase of meningioma remains controversial. The effects of surgery and the factors associated with postsurgical complications and patient prognosis were studied to optimize surgical decisions for clinicians who treat asymptomatic patients. The medical records of 513 patients with meningiomas (112 patients were asymptomatic) treated at our hospital from May 2007 to April 2012 were retrospectively reviewed. The results were analyzed with univariate and multivariate analyses. Asymptomatic meningiomas were characterized by a more common cerebral hemispheric location, a smaller size, and a lack of peritumoral edema. A significantly higher Simpson I resection rate of 95.2 % was achieved in tumors located in the cerebral hemisphere; in contrast, a rate of 66.7 % was obtained in tumors located at the skull base (P = 0.003). The overall postsurgical complication rate was 13.6 %, which was lower than the rate of 21.7 % in the symptomatic patients. Hemiplegia was the most common complication, which occurred most often in the patients with tumors in parietal locations (P = 0.015). Ninety-two percent of the asymptomatic patients achieved a Glasgow Outcome Scale (GOS) score of 5 1 year after the operation, and significantly more patients younger than 60 years of age obtained a GOS score of 5 compared with patients older than 60 years of age (P = 0.006). To achieve maximal tumor resection and good patient recovery, tumor location and patient age should be carefully considered prior to choosing to perform surgery in asymptomatic patients.
    Neurosurgical Review 02/2015; · 1.86 Impact Factor
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    ABSTRACT: Leucine-rich repeats and immunoglobulin-like domains (LRIG) 3 gene is mapped to chromosome 12q13.2, a region that is frequently deleted in a subset of glioblastoma multiforme (GBM). It has been reported that perinuclear LRIG3 staining correlated with low WHO grade of glioma and better survival of the patients. However, the relationship between LRIG3 and glioma is not very clear. The purpose of this study is to demonstrate the impacts of LRIG3 on biological characteristics of glioma and its possible mechanisms. We found that transduction of LRIG3 into glioblastoma cells inhibited cell growth in vitro and in vivo, promoted cell apoptosis, and restrained cell invasion and migration. Further studies demonstrated that LRIG3 negatively regulated the epidermal growth factor receptor (EGFR) signaling pathway. Inhibition of EGFR could reduce the effects of LRIG3 knockdown on cell proliferation and EGFR signaling pathway. In conclusion, LRIG3 functions as a tumor suppressor by attenuating EGFR signaling pathway and the restoration of LRIG3 may offer therapeutic potential against malignant gliomas. Copyright © 2015 Elsevier B.V. All rights reserved.
    Journal of the neurological sciences. 02/2015;
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    ABSTRACT: Similar histology and clinical behavior of both intraventricular central neurocytomas (CNs) and extraventricular neurocytomas (EVNs) may argue against the idea that EVNs were the distinct entity to distinguish from CNs in the 2007 World Health Organization classification. To explore respective characteristics and compare similarities and differences in CNs and EVNs, relevant clinical, radiological, operative and pathological data of 49 patients (35 CNs and 14 EVNs) in the Department of Neurosurgery at our hospital from 2005 to 2012 was reviewed and some comparisons between CNs and EVNs were conducted. The factors affecting posttreatment recurrence of CNs and EVNs were assessed by Cox regression analysis. In comparison, CNs showed a more typical clinical manifestation, and radiological and histopathological features, while EVNs demonstrated more malignant biological behavior, with higher MIB-1 index (p = 0.006), higher rate of atypia (p = 0.042), higher recurrence rate (p = 0.028), and shorter time to recurrence (p = 0.049). Subtotal resection was associated with higher rates of recurrence in both CNs (hazard ratio [HR] 6.16, p = 0.046) and EVNs (HR 5.26, p = 0.045), and atypia was also associated with a higher recurrence rate in CNs (HR 5.03, p = 0.042). CNs were thus easier to diagnose than EVNs, with typical clinical, radiological, and histopathological features, while the latter were more likely to show malignant biological behavior associated with atypia and recurrence. Total surgical resection is the optimal treatment choice for both CNs and EVNs, and patients with either CN or EVN with typical and/or totally resected lesions showed favorable clinical outcomes.
    Journal of Neuro-Oncology 11/2014; 121(3). · 3.12 Impact Factor
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    ABSTRACT: The human leucine-rich repeats and immunoglobulin-like domains (LRIG) gene family contains LRIG1, 2 and 3, encoding integral membrane proteins with an ectodomain, a transmembrane domain and a cytoplasmic tail. LRIG1 negatively regulates multiple receptor tyrosine kinases signaling including the epidermal growth factor receptor (EGFR) and is a proposed tumor suppressor. The soluble LRIG1 ectodomain is demonstrated to be shed naturally and inhibit the progression of glioma. However, little is known regarding the functions of LRIG2. In oligodendroglioma, LRIG2 expression is associated with poor survival, suggesting that LRIG2 might have different functions compared with LRIG1. Since soluble LRIG1 ectodomain has a similar function to the full-length LRIG1, we hypothesize that the different roles exerted by LRIG2 and LRIG1 result from the difference of their ectodomains. Here, we addressed the functions of LRIG2 and LRIG2 ectodomain in the proliferation and apoptosis of glioma and the possible underlying mechanisms. Firstly, we found that LRIG2 expression levels positively correlated with the grade of glioma. Further, we demonstrated for the first time that soluble LRIG2 ectodomain was capable of being released from glioblastoma cells and exerted a pro-proliferative effect. Overexpression of LRIG2 ectodomain promoted the proliferation and inhibited the apoptosis of glioblastoma cells in vitro and in vivo in a similar manner to the full-length LRIG2. Both full-length LRIG2 and LRIG2 ectodomain were found to physically interact with EGFR, enhance the activation of EGFR and its downstream PI3 K/Akt pathway. To our knowledge, this is the first report demonstrating that soluble LRIG2 ectodomain is capable of being released from glioblastoma cells and exerts a similar role to the full-length LRIG2 in the regulation of EGFR signaling in the progression of glioblastoma. LRIG2 ectodomain, with potent pro-tumor effects, holds promise for providing a new therapeutic target for the treatment of glioblastoma.
    PLoS ONE 10/2014; 9(10):e111419. · 3.53 Impact Factor
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    ABSTRACT: Mesenchymal stem cells (MSCs) and neural progenitor cells (NPCs) have been regarded for their clinical therapeutic potential for central nervous system (CNS) pathologies. Their potential utility is a result of their intrinsic ability to repair damaged tissues, deliver therapeutic proteins and migrate to sites of pathology within the brain. However, it remains unclear whether the CNS promotes any changes in these potential therapeutic cells, which would be critical to understand before clinical application. A major component of the CNS is cerebrospinal fluid (CSF). Therefore, the aim of this study was to evaluate the influence that human CSF has on the function of human adipose-derived MSCs (hAMSCs) and human fetal-derived NPCs (hfNPCs) in regards to cell proliferation, survival, and migration. This study demonstrated that human CSF promoted proliferation and inhibited apoptosis of hAMSCs and hfNPCs. Pre-culturing these stem cells in human CSF also increased their migratory speed and distance traveled. Furthermore, IGF-1 in human CSF enhanced the migration capacity and increased the expression of C-X-C chemokine receptor type 4 (CXCR4) in both stem cell types. These current findings highlight a simple and natural way in which human CSF can enhance the proliferation, migration and viability of both hAMSCs and hfNPCs. This study may provide insight into improving the clinical efficacy of stem cells for the treatment of CNS pathologies.
    Stem Cells and Development 09/2014; 24(2). · 4.20 Impact Factor
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    ABSTRACT: Glioma stem cells (GSCs), characterized by self-renewal, multi-potentiality and tumorigenicity, are responsible for the tumor propagation, recurrence and resistance to traditional treatments, representing a critical therapeutic target. Neural stem cells (NSCs) possess inherent tropism to brain tumor cells and inhibit their growth. However, there is a limited understanding of the mechanism underlying NSC tropism and the effect of NSC migration on GSC stemness phenotypes. In the present study, we showed that GSCs exhibited enhanced chemotaxis for NSC tropism compared with their differentiated cells. Chemokines secreted by GSCs contributed to the targeted migration of NSCs. Hypoxia enhanced NSC tropism via the upregulated chemokine expression of GSCs, such as VEGF, EGF and bFGF. In vitro migration of NSCs induced GSC differentiation and reduced stem-like phenotypes. Moreover, in vivo data provided direct evidence that transplanted NSCs could migrate to GSCs from either the homolateral or contralateral brain injection site, which prolonged the survival of grafted mice. Taken together, these findings show that NSCs preferentially migrate to GSCs and reduce their stemness phenotypes, raising the intriguing possibility that the targeted migration of NSCs can be applied as a novel therapeutic strategy to target these intractable brain tumors.
    International journal of oncology. 08/2014;
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    ABSTRACT: Glioblastoma, a highly lethal brain tumor, features extensive heterogeneity at the cellular and molecular levels. The discovery of glioma stem cells (GSCs) supports a new paradigm in tumor biology and therapeutic targeting. GSCs contribute to the cellular origin of primary gliomas and the recurrence of malignant gliomas after traditional treatments. A growing body of evidence suggests that GSCs, just as the bulk tumor cells, are heterogeneous with phenotypic and genetic complexity. Heterogeneous GSCs may add to glioblastoma heterogeneity and impact response to current therapies. A better understanding of GSC heterogeneity is required to facilitate the design of more effective therapies against this highly malignant brain tumor.
    Current Signal Transduction Therapy 08/2014; 9(2). · 0.45 Impact Factor
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    ABSTRACT: Glioblastoma, the most common and lethal type of intracranial tumor, is characterized by extensive heterogeneity at the cellular and molecular levels. The discovery of glioma stem cells (GSCs) lends support to a new paradigm in tumor biology. In the present study, we aimed to clarify the validity of using U251 glioma cells as a source of GSC culture and critically evaluate the heterogeneous stem-like phenotypes of these cells when grown under various culture conditions. The findings suggested that U251 cells (U251-Adh, U251-SC-Sph and U251-SC-Adh) showed distinctive growth patterns and self-renewal capacity. The U251 glioma cell line is endowed with certain GSC phenotypes that may be moderately enriched in vitro when transferred into stem cell culture conditions, although this is not sustainable and reproducible in vivo. Notably, glioma cells are plastic in response to their environment. The reversible adaptive plasticity contributes to the GSC heterogeneity, which may lead to the heterogeneity of glioblastoma and the differing responses to current therapies. Therefore, an improved understanding of GSC heterogeneity is urgently required for designing more effective therapies against this highly malignant brain tumor.
    Oncology letters 12/2013; 6(6):1649-1655. · 0.99 Impact Factor
    This article is viewable in ResearchGate's enriched format
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    ABSTRACT: Extraventricular neurocytomas (EVNs) are rare neuronal tumors included in the definition of neoplasms in the 2007 World Health Organization classification of tumors of the central nervous system. Although a small case series of EVNs in adults has been previously reported, EVNs in pediatric populations are extremely rare. The current case report presents the clinicopathological features of an EVN in a 2-year-old female who presented with nausea and vomiting that had lasted for five days. In addition, an analysis of the imaging features, histology, treatment and prognosis of these reported rare lesions is presented. Immunohistochemically, EVNs are characterized by the robust expression of synaptophysin, but with a lack of oligodendrocyte transcription factor 2, isocitrate dehydrogenase enzyme isoform 1 (IDH1) R132/IDH2 R172 mutations and p53 immunoexpression. The treatment for EVNs in pediatric and adult populations is gross total resection, with post-operative radiation reserved for subtotal resection or recurrent disease. In addition, drop metastasis must be carefully avoided.
    Oncology letters 11/2013; 6(5):1397-1405. · 0.99 Impact Factor
    This article is viewable in ResearchGate's enriched format
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    ABSTRACT: Accumulating evidence indicates that extensive microglia activation-mediated local inflammation contributes to neuronal injury in cerebral ischemia. We have previously shown that 4-(2-butyl-6, 7-dichloro-2-cyclopentyl-indan-1-on-5-yl) oxobutyric acid (DCPIB), a potent volume-regulated anion channel (VRAC) inhibitor, suppresses pathological glutamate release and excitatory neurotoxicity in reversible middle cerebral artery occlusion (rMCAO) model in vivo. In the present study, we sought to determine whether DCPIB also attenuates microglia activation that could contribute to neuronal injury in the cerebral ischemia/reperfusion pathology. We show that oxygen-glucose deprivation (OGD) induced microglia proliferation, migration, and secretion of cytokines and all these pathological changes were effectively inhibited by DCPIB in vitro. In the microglia/neuron co-cultures, OGD induced neuronal damage was reduced markedly in the presence of DCPIB. In rat rMCAO animal model, DCPIB significantly attenuated microglia activation and neuronal death. Activation of mitogen-activated protein kinase (MAPK) signaling pathway is known to be a critical signaling pathway for microglia activation. We further explored a potential involvement of DCPIB in this pathway by western blot analysis. Under the conditions that MAPK pathway was activated either by lipopolysaccharides (LPS) or OGD, the levels of phosphorylated ERK1/2, JNK and p38 were reduced significantly in the presence of DCPIB. Altogether, our study demonstrated that DCPIB inhibits microglia activation potently under ischemic conditions both in vitro and in vivo. The DCPIB effect is likely attributable to both direct inhibition VRAC and indirect inhibition of MAPK pathway in microglia that are beneficial for the survival of neurons in cerebral ischemic conditions.
    Brain research 11/2013; · 2.83 Impact Factor
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    ABSTRACT: Studies have demonstrated that embryonic cell therapy is a potential approach for the treatment of Huntington's disease (HD). However, because of the limited resource of embryos, greater attention is needed in developing more efficient surgical techniques that not only enhance the therapy outcome but also avoid inefficient therapeutics of transplantation. In this study, we explored the curative effects of two different transplantation methods using a rat model of HD. Whole ganglionic eminence (WGE) cells or phosphate-buffered saline were transplanted into unilateral striatum of quinolinic acid (QA)-lesioned rats using microtransplantation instruments (with an outer diameter of 50 μm) or traditional transplantation instruments (with an outer diameter of 470 μm). Apomorphine-induced rotation test and adjusting step test were assessed after QA-induced lesion and 2, 4, 6, 8, 10, and 12 weeks after transplantation. The expression of neuronal nuclei (NeuN), dopamine, cAMP-regulated phosphoprotein of molecular weight 32 kDa (DARPP-32), and glial fibrillary acidic protein (GFAP) was analyzed at 12 weeks after transplantation. We observed that microtransplanted rats performed better in the stepping test and had higher numbers of DARPP-32-positive cells compared with traditionally transplanted rats. Moreover, microtransplantation group showed lower GFAP expression surrounding the grafts in unilateral striatum and a higher survival rate posttransplantation compared with the traditional transplantation group. We conclude that microtransplantation is capable of enhancing therapeutic efficacy in the rat model of HD. This finding establishes the basis of an alternative transplantation strategy for treatment of HD. © 2013 Wiley Periodicals, Inc.
    Journal of Neuroscience Research 09/2013; · 2.73 Impact Factor
  • Qinglei Gao, Ting Lei, Fei Ye
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    ABSTRACT: Introduction: The highly divergent histological heterogeneities, aggressive invasion and extremely poor response to treatment make glioblastoma (GBM) one of the most lethal and difficult cancers in humans. Among key elements driving its behavior is epidermal growth factor receptor (EGFR), however, neither traditional therapy including neurosurgery, radiation, temozolomide, nor targeted EGFR therapeutics in clinic has generated promising results to date. Strategies are now focusing on blocking the downstream EGFR-activated metabolic pathways and the key phosphorylated kinases. Areas covered: Here, we review two major EGFR-activated downstream metabolic pathways including the PI3K/AKT/mTOR and RAS/RAF/MAPK pathways and their key phosphorylated kinase alterations in GBMs. This review also discusses potential pharmacological progress from bench work to clinical trials in order to evaluate specific inhibitors as well as therapeutics targeting PI3K and RAS signaling pathways. Expert opinion: Several factors impede clinical progress in targeting GBM, including the high rates of acquired resistance, heterogeneity within and across the tumors, complexity of signaling pathways and difficulty in traversing the blood-brain barrier (BBB). Substantial insight into genetic and molecular pathways and strategies to better tap the potential of these agents include rational combinatorial regimens and molecular phenotype-based patient enrichment, each of which will undoubtedly generate new therapeutic approaches to combat these devastating disabilities in the near future.
    Expert Opinion on Investigational Drugs 06/2013; · 4.74 Impact Factor
  • Acta Neurochirurgica 05/2013; 155(8). · 1.79 Impact Factor
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    ABSTRACT: To determine appropriate protocols for the identification and management of intra operative suspicious tissues during transsphenoidal surgery. Clinical data and pathological reports of 20 patients with intra-operative suspicious tissues during transsphenoidal surgeries were analyzed retrospectively. The methods for discriminating between adenoma and normal pituitary tissues were reviewed. The postoperative pathological reports revealed that adenoma and normal pituitary tissues coexisted in 9 samples, while 5 samples were identified as normal pituitary tissues, 2 as adenoma tissues, and 4 as other tissues. Adenomas were distinguished from normal pituitary tissues on the basis of intra-operative appearance, texture, blood supply and possible existence of boundary. If decisions are difficult to made during surgeries from the appearance of the suspicious tissues, pathological examinations are advised as a guidance for the next steps.
    Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 05/2013; 44(3):441-3.
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    ABSTRACT: The molecular mechanisms that drive the develop-ment and aggressive progression of malignant astrocytic tumors remain obscure. Recently, in the search for endo-genous negative regulators of EGF receptor, LRIG1 was cloned and characterized as a putative tumor suppressor gene often downregulated in various human tumors, including astrocytic tumors. Although several studies have implicated the function of LRIG1 in the inhibition of tumorigenesis, its precise role and potential underlying mechanisms remain obscure. Therefore, we generated a full-length expression vector to overexpress LRIG1 in the U251 malignant glioma cell line. Introduction of exogenous LRIG1 into glioma cells inhibited cell proliferation manifested by MTT and soft agar clone assay in vitro and subcutaneously tumor xenografts. On the other hand, LRIG1 overexpression inhibited glioma growth by significantly changing the expression pattern of cyclins, resulting in delayed cell cycle. Employing transwell invasion and wound scratch assay and gelatin zymography, LRIG1 inhibited U-251 MG cell invasion and migration by attenuating MMP2 and MMP9 production. Under ligand-stimulated conditions, p-ERK levels did not change, whereas p-AKT levels were inhibited in cells with LRIG1 upregulation, indicating that LRIG1 exerts more inhibiting effects on the PI3K/AKT pathway. Our findings suggest that LRIG1 restricted glioma aggressiveness by inhibiting cell proliferation, migration and invasion. Restoration of LRIG1 to glioma cells could offer a novel therapeutic strategy.
    International Journal of Oncology 01/2013; · 2.77 Impact Factor
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    ABSTRACT: To explore the effects of all-trans retinoic acid (ATRA) on glioma stem cell phenotype. The glioma stem cell (GSC) from surgically resected human glioma specimens were isolated and enriched by neurosphere assay and then its differentiation was induced with all-trans retinoic acid (ATRA, 1 µmol/L) for 1 week. Markers were determined by flow cytometry, Western blot and reverse transcription-polymerase chain reaction (RT-PCR). Side population cells were analyzed by flow cytometry. Growth characteristics were detected by neurosphere formation assay and cell cycle analysis. GSC and the differentiated cells (1×10(5)) were implanted stereotactically and intracranially into the Balb/c nude mice to compare the survival time. All data were analyzed with the SPSS software version 17.0. ATRA potently induced the differentiation of GSC and reduced glioma stem cell phenotype. And there were an elevated expression of glial fibrillary acidic protein (GFAP) and a reduced expression of such stem cell makers as CD133 and Nestin. The side population rate decreased. ATRA inhibited the neurosphere formation of GSC and induced the arrest of cell growth. ATRA could prolong the survival time. GSC may be differentiated efficiently by ATRA. The stemness of GSC decreases obviously after the differentiation of ATRA and the survival time is prolonged. Thus ATRA may be applied for targeted therapies of glioma stem cell.
    Zhonghua yi xue za zhi 01/2013; 93(1):19-22.
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    ABSTRACT: Clear cell hidradenocarcinoma (CCH) is an exceedingly rare and highly malignant tumor of the eccrine sweat glands. Its treatment is extremely difficult due to the characteristically aggressive clinical course including repeated local recurrence and uncontrollable distal metastasis coming along with a very poor prognosis. Most published case studies recommend a wide surgical excision followed by adjuvant conservative therapy, which is generally considered to be the standard treatment. Two cases of nodular CCH of the scalp either presenting as a singular primary lesion or at an already metastatic stage were analyzed retrospectively. Wide local excision of the tumor couldn't prevent the primary carcinoma from recurring and metastasizing. Both cases received various therapies but the results were unsatisfactory. Although most authors have recommended that early wide surgical excision of the tumor is a feasible therapeutic measurement, our results raise doubts on the efficacy of this treatment strategy. As alternative approaches (i.e. chemotherapy, radiotherapy) are similarly controversial, further studies and a wide exchange of clinical experiences are crucial.
    Journal of Huazhong University of Science and Technology 12/2012; 32(6):931-6. · 0.78 Impact Factor
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    ABSTRACT: The LRIG1 [leucine-rich repeats and immunoglobulin-like domains (LRIG)] gene is not universally downregulated in human cancers, and its role in tumorigenesis and the development of glioma has not been well addressed. In this study, we used short hairpin RNA (shRNA)-triggered RNA interference (RNAi) to block LRIG1 gene expression in the GL15 human glioma cell line. Specific downregulation of LRIG1 by shRNA resulted in significantly enhanced capabilities of proliferation, inhibition of apoptosis and invasion in the GL15 cells. LRIG1 repression induced marked activation of epidermal growth factor receptor (EGFR), protein kinase B (Akt) and c-Myc signaling molecules. Our results demonstrated that RNAi against LRIG1 may effectively downregulate LRIG1 gene expression. LRIG1 functions as a tumor suppressor in the pathogenesis of glioma via EGFR/Akt/c-Myc activation.
    Oncology Reports 10/2012; · 2.19 Impact Factor
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    ABSTRACT: The mortality of patients with malignant gliomas remains high despite the advancement in multi-modal therapy including surgery, radio- and chemotherapy. Glioma stem cells (GSCs), sharing some characteristics with normal neural stem cells (NSCs), contribute to the cellular origin for primary gliomas and the recurrence of malignant gliomas after current conventional therapy. Accordingly, targeting GSCs proves to be a promising avenue of therapeutic intervention. The specific tropism of NSCs to GSCs provides a novel platform for targeted delivery of therapeutic agents. Tropism and mobilization of NSCs are enhanced by hypoxia through upregulating chemotactic cytokines and activating several signaling pathways. Moreover, hypoxia-inducible factors (HIFs) produced under hypoxic microenvironment of the stem cell niche play critical roles in the growth and stemness phenotypes regulation of both NSCs and GSCs. However, the definite cellular and molecular mechanisms of HIFs involvement in the process remain obscure. In this review, we focus on the pivotal roles of HIFs in migration of NSCs to GSCs and potential roles of HIFs in dictating the fates of migrated NSCs and targeted GSCs.
    Neurochemical Research 09/2012; · 2.55 Impact Factor
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    ABSTRACT: LRIG family shares similar structures that include a signal peptide, an extracellular region consisting of a leucine-rich repeat domain and three immunoglobulin-like domains, a transmembrane domain, and a cytoplasmic tail. After activation of EGFR, the extracellular LRR domain and immunoglobulin-like domains of LRIG1 can bind to the extracellular parts of EGFR, resulting in recruitment of c-Cbl to the cytoplasmic domains, and induction of EGFR degradation. This study investigated the effects of overexpression of leucine-rich repeats and LRIG1 on cisplatin (CDDP) sensitivity in the glioma cell line U251 and explored the possible mechanisms mediating this effect. We found that CDDP could inhibit the growth of U251 cell line and induced activation of the EGFR. Overexpression of LRIG1 increased the inhibitory effect of CDDP on the U251 cell line via the inhibition of proliferation and induction of apoptosis. The mechanisms underlying the effect of the combined treatment of LRIG1 and CDDP could be that LRIG1 blocked CDDP-induced EGFR activation and regulated the apoptosis proteins. These findings suggest that upregulation of LRIG1 expression enhances the CDDP sensitivity in the glioma cell line U251.
    Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics 05/2012; 20(5-6):205-11. · 0.92 Impact Factor

Publication Stats

501 Citations
140.72 Total Impact Points

Institutions

  • 1997–2014
    • Tongji Hospital
      Wu-han-shih, Hubei, China
  • 2012
    • China Three Gorges University
      Tung-hu, Hubei, China
  • 2004–2012
    • Huazhong University of Science and Technology
      • Department of Neurosurgery
      Wuhan, Hubei, China
  • 2008
    • Zhejiang University
      • School of Medicine
      Hangzhou, Zhejiang Sheng, China
  • 2005
    • Henan Provincial People’s Hospital
      Cheng, Henan Sheng, China
  • 1997–1999
    • Tongji Medical University
      • Department of Pediatrics
      Wu-han-shih, Hubei, China
  • 1995–1996
    • Friedrich-Alexander Universität Erlangen-Nürnberg
      • Department of Neurology
      Erlangen, Bavaria, Germany