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1.
Int Immunopharmacol ; 79: 106175, 2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-31918060

RESUMO

Acute lung injury (ALI) is one of the severe complications in patients with traumatic brain injury (TBI), contributing to the high mortality. Ghrelin has protective effects against various inflammatory diseases, but the effects of Ghrelin on TBI-induced ALI and its mechanisms remain unknown. In this study, Ghrelin administration was performed on the mice with TBI, then histological change in cortex and lung tissues, lung vascular permeability and macrophage number in bronchoalveolar lavage fluid (BALF) were examined, respectively. Simultaneously, the alterations of proinflammatory factors and pyroptosis-related proteins in lung tissues were detected. As a result, TBI-induced ALI was ameliorated after Ghrelin treatment, which was demonstrated by improved histology, reduced lung vascular permeability, and peripheral macrophage number. Furthermore, Ghrelin decreased the mRNA levels of proinflammatory factors (IL-1ß, IL-6, TNF-α and IL-18), the protein levels of pyroptosis-related proteins (NLRP3, Caspase1-P20, HMGB1 and Gasdermin D), and the phosphorylation levels of NF-κB in lung tissues. These results showed that Ghrelin attenuating TBI-induced ALI might be via ameliorating inflammasome-induced pyroptosis by blocking NF-κB signal, which are important for the prevention and treatment of TBI-induced ALI.

2.
Pathol Res Pract ; 216(2): 152790, 2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-31864713

RESUMO

BACKGROUND: Glioma is the most common primary malignant tumor with poor prognosis due to the lack of understanding the mechanism underlying the disease and the early diagnosis indexs. It is necessary to identify molecular signatures for predicting the overall prognosis of glioma. Adipocyte enhancer binding protein1 (AEBP1) acts as a transcriptional repressor and plays a role in adipogenesis and smooth muscle cell differentiation. However, its role in glioma remains unclear. MATERIALS AND METHODS: AEBP1 expression was analyzed by bioinformatics using the public database and by qPCR and western blotting in human glioma tissues. AEBP1 downregulation was performed by lipofectamine3000-mediated siRNA transfection. Cell proliferation and invasion were determined by cell counting kit-8 and transwell assays, while early cell apoptosis was determined by flow cytometry. The proteins of downstream NF-κB signaling pathway were determined by western blotting. RESULTS: AEBP1 is highly expressed in human gliomas. Lipofectamine 3000-mediated siRNA transfection stably and efficiently suppressed AEBP1 mRNA and protein expression in human glioma cells. AEBP1 downregulation inhibited cell proliferation and invasion, but promoted early cell apoptosis. Also, AEBP1 knockdown in glioma cells decreased the expression of NF-κB1. Furthermore, the downstream of NF-κB signaling pathway, Bax, caspase-3 are increased, while MMP2 and Bcl-2 are decreased in glioma cells. CONCLUSION: Elevated AEBP1 is positively associated with poor prognosis of glioma. AEBP1 downregulation suppressed cell proliferation and invasion, but promoted early cell apoptosis. AEBP1 downregulation suppressed the cell proliferation and invasion may by inhibiting the NF-κB signaling pathway.

3.
J Craniofac Surg ; 30(7): 2239-2244, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31503116

RESUMO

BACKGROUND: A skull fracture widely occurs in patients with traumatic brain injury, leading to intracranial hematoma, brain contusion, and intracranial infection. It also influences the prognosis and death of patients. This study aimed to discuss cases of patients with comminuted skull fractures. METHODS: From October 2015 to December 2018, 38 patients with comminuted skull fractures were admitted to the hospital. All patients underwent three-dimensional reconstruction of computed tomography scan images. Digital subtraction angiography or magnetic resonance venography was performed to find out the venous sinus. The clinical findings of the patients were significant regarding gender, age, injury mechanism, location, admission Glasgow Coma Scale (GCS), combined epidural, subdural, cerebral contusion, intracranial pneumatosis, maximum depth of depression, admission to surgery, dural tear, post-operative cerebrospinal fluid leakage, post-operative infection, and Glasgow Outcome Scale (GOS) 3 months after surgery. RESULTS: The incidence of traffic accidents, fall from a height, railway accidents, fall of an object, and chop injury was 60.5%, 18.4%, 13.2%, 5.3%, and 2.6%, respectively. Intra-operative dural trar negatively correlated with epidural hematoma, cerebral contusion, and subdural hematoma. Also, post-operative infection negatively correlated with intracranial pneumatosis, depth of fracture depression, and pre-operative cerebrospinal fluid leakage. No correlation was found between contusion, subdural hematoma, intracranial pneumatosis, depth of fracture depression, and post-operative infection. The GOS score positively correlated with age, pre-operative cerebrospinal fluid leakage, and admission GCS score. CONCLUSIONS: A perfect pre-operative examination is a key to successful surgery. Further studies should be conducted to find out more effective treatments for traumatic comminuted skull fractures.


Assuntos
Fratura do Crânio com Afundamento/cirurgia , Adulto , Idoso , Idoso de 80 Anos ou mais , Vazamento de Líquido Cefalorraquidiano/etiologia , Contusões , Feminino , Escala de Coma de Glasgow , Humanos , Masculino , Pessoa de Meia-Idade , Fratura do Crânio com Afundamento/complicações , Fratura do Crânio com Afundamento/diagnóstico por imagem , Tomografia Computadorizada por Raios X , Resultado do Tratamento , Adulto Jovem
4.
Biochem Biophys Res Commun ; 509(1): 182-187, 2019 01 29.
Artigo em Inglês | MEDLINE | ID: mdl-30587343

RESUMO

BACKGROUND: Glioma is the most common malignancy in brain carcinoma with poor prognosis due to the lack of understanding of the mechanism underlying the disease. γ-interferon-inducible lysosomal thiol reductase (GILT) plays a critical role in the process of antigen processing. However, the role of GILT in the tumorigenesis of glioma remains unknown. MATERIALS AND METHODS: The expression of GILT was analyzed by bioinformatics using the public database and by qPCR in three human glioma cell lines. Cell growth and viability were determined by Celigo and MTT assays, while cell cycle arrest and apoptosis were determined using flow cytometry. Giemsa staining was used to analyze the colony formation, while cell motility was assessed using transwell migration and invasion assays, as well as, using tumor growth in nude mice. RESULTS: GILT was highly expressed as observed in the public database on human gliomas and two human glioma cell lines, U373MG and U87MG cells. The downregulation of GILT by lentiviral-mediated silencing inhibits the cell growth, colony formation, and migration but promotes apoptosis and results in cell cycle arrest at the G0/G1 phase in the U373MG cells. Also, the knockdown of GILT inhibits tumor growth in vivo. CONCLUSION: Elevated GILT is positively associated with glioma progression. GILT silencing suppresses cell proliferation, colony formation, migration, and tumor growth, and induces apoptosis and cell cycle arrest. GILT may serve as a potential target for the treatment of glioma.


Assuntos
Neoplasias Encefálicas/genética , Carcinogênese/genética , Proliferação de Células , Regulação Neoplásica da Expressão Gênica , Glioma/genética , Oxirredutases atuantes sobre Doadores de Grupo Enxofre/genética , Animais , Apoptose , Neoplasias Encefálicas/patologia , Carcinogênese/patologia , Pontos de Checagem do Ciclo Celular , Linhagem Celular Tumoral , Regulação para Baixo , Feminino , Técnicas de Silenciamento de Genes , Glioma/patologia , Humanos , Lentivirus/genética , Camundongos Endogâmicos BALB C , Camundongos Nus
5.
Oncol Rep ; 40(6): 3285-3296, 2018 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-30272353

RESUMO

Glioma is the most common adult malignant primary brain tumor; however, the effect of chemotherapy is often limited by drug­resistance and poor prognosis is common. Ring finger protein 138 (RNF138) belongs to the E3 ligase family, and has significantly higher expression level in glioma tissue than in noncancerous brain tissues. Epithelial-mesenchymal-transition (EMT) has a critical role in cancer invasion and metastasis, ultimately leading to increased cell motility and resistance to genotoxic agents. Extracellular­signal regulated kinase (Erk) pathways promote the growth of glioma cells and enhance tumor invasion, with a role in the progression of EMT. However, the association between RNF138 and human glioma progression remains poorly understood. Relatively little is known about the association between RNF138, Erk, and EMT in glioma progression. In the current study, experiments were performed to explore the potential roles and mechanisms of RNF138 in glioblastoma in vitro and in vivo. Glioma cell line proliferation, migration and invasion were inhibited by knockdown of RNF138 in vitro. By lowering the RNF138 expression, cleaved caspase3 and E­cadherin were upregulated, while phospho­Erk1/2, vimentin, MMP2, HIF­1α and VEGF were downregulated in U87 and U251 cells in vitro. In vivo findings revealed that the growth of U87 cell­transplanted tumors in nude mice was inhibited in tumors with RNF138 knockdown. These findings suggested that downregulation of RNF138 inhibited glioma cell proliferation, migration, and invasion, and reversed EMT, potentially via Erk signaling pathway. Therefore, RNF138 may be a potential therapeutic target against glioma.


Assuntos
Neoplasias Encefálicas/genética , Regulação para Baixo , Transição Epitelial-Mesenquimal , Glioblastoma/genética , Ubiquitina-Proteína Ligases/genética , Animais , Neoplasias Encefálicas/metabolismo , Linhagem Celular Tumoral , Movimento Celular , Proliferação de Células , Progressão da Doença , Regulação Neoplásica da Expressão Gênica , Glioblastoma/metabolismo , Humanos , MAP Quinase Quinase Quinase 3 , Camundongos , Camundongos Nus , Invasividade Neoplásica , Transplante de Neoplasias , Ubiquitina-Proteína Ligases/metabolismo
6.
Front Neurosci ; 12: 445, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30026681

RESUMO

Traumatic brain injury (TBI) is a primary cause of disability and mortality. Ghrelin, a gastrointestinal hormone, has been found to have protective effects for the brain, but the molecular mechanism of these neuroprotective effects of ghrelin remains unclear. In this study, an electronic cortical contusion impactor was used to establish a rat TBI model and we investigated the effect of ghrelin on brain repair by neurological severity score and histological examination. An antibody array was employed to uncover the molecular mechanism of ghrelin's neuroprotective effects by determining the alterations of multiple proteins in the brain cortex. As a result, ghrelin attenuated brain injury and promoted brain functional recovery. After TBI, 13 proteins were up-regulated in the brain cortex, while basic fibroblast growth factor (bFGF) and fibroblast growth factor-binding protein (FGF-BP) were down-regulated after ghrelin treatment. It is known that bFGF can induce angiogenesis in the brain and accelerate wound healing, which can be further enhanced by FGF-BP. Based on the previous studies, it is hypothesized that the exogenous ghrelin curing TBI might cause the closure of bFGF and FGF-BP functions on wound healing, or ghrelin might exert the neuroprotective effects by competitively inhibiting bFGF/FGF-BP-induced neovascularization. Whether the combinational administration of ghrelin and bFGF/FGF-BP can enhance or weaken the therapeutic effect on TBI requires further research.

7.
Front Neurol ; 8: 560, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-29250024

RESUMO

Objective: Traumatic brain injury (TBI) occurs commonly in children. Repeat computed tomography (CT) follow up of TBI patients is often scheduled to identify progressive hemorrhagic injury (PHI). However, the utility of repeated CT scans, especially in children with mild TBI [Glasgow Coma Scale (GCS) scores of 13-15], has been debated. The purposes of the present study were to identify clinical predictors of PHI in children with mild TBI and to clarify relevant clinical factors via radiological examination. Methods: From 2014 to 2016, we retrospectively enrolled children <15 years of age with mild TBI. We recorded age, sex, GCS scores on admission, causes of head injury, timing of initial CT, any loss of consciousness, vomiting and seizure data, and type of TBI. Based on repeat CT findings, patients were dichotomized into either a PHI group or a non-PHI group. Also, clinical data were comparatively reviewed. Multivariate logistic regression analysis was used to identify clinical predictors of PHI. Results: Of the 175 enrolled children, 15 (8.6%) experienced PHI. Univariate analysis revealed that GCS score on admission, cause of head injury, vomiting, seizure, and TBI type were associated with PHI. Multivariate logistic regression analysis showed that a GCS score of 13 and epidural hemorrhage (EDH) were independently associated with PHI (hazard ratio = 0.131, P = 0.018; hazard ratio = 6.612, P = 0.027, respectively). Conclusion: A GCS score of 13 and EDH were associated with PHI. These factors should be considered when deciding whether to repeat CT on children with mild TBI.

8.
Oncotarget ; 8(54): 92615-92620, 2017 Nov 03.
Artigo em Inglês | MEDLINE | ID: mdl-29190942

RESUMO

Purpose: Mild traumatic brain injury (TBI) is common in children. The aim of this study was to identify clinical predictors of intracranial injuries on computed tomography (CT) in infants younger than 2 years old with mild TBI, which allow reducing number of imaging. Results: Of 214 enrolled infants with complete data, 30 (5.8%) sustained intracranial injuries. Younger age in months, severe injury mechanism and scalp hematomas were associated with traumatic intracranial injuries on CT. 71 had scalp hematomas and 143 had no scalp hematoma. Within infants with scalp hematomas, 26 sustained intracranial injuries and 45 presented normal. Intracranial injuries were significantly correlated with larger scalp hematomas and different scalp hematoma locations. Logistic regression analysis showed that scalp hematoma and mechanism of injury in infants younger than 2 years old with mild TBI was related to intracranial injuries (hazard ratio=38.291, P=0.0001; hazard ratio=0.174, P=0.001). In subgroup of mild TBI infants with scalp hematomas, logistic regression analysis showed age, scalp hematoma size and mechanism of injury were independently associated with intracranial injuries (hazard ratio=0.299, P=0.032; hazard ratio=5.272, P=0.006; hazard ratio=0.312, P=0.030). Methods: Between 2014 and 2016, we retrospectively enrolled infants <2 years old with mild TBI. Data recorded included age, sex, mechanism of head injury, size and location of scalp hematoma, fracture and intracranial injuries on CT. Conclusion: The characteristics of scalp hematomas and mechanism of injury were associated with intracranial injuries. These factors should be considered when making decisions on radiologic examinations of infants < 2 years old with mild TBI and alternative procedures, which do not involve ionizing radiation, should be used if appropriate.

9.
Zhonghua Zhong Liu Za Zhi ; 35(10): 726-31, 2013 Oct.
Artigo em Chinês | MEDLINE | ID: mdl-24378091

RESUMO

OBJECTIVE: To study the phenotype and tumorigenicity of SHG-44 glioma stem cell spheres and the pathological characteristics of their xenograft tumors. METHODS: SHG-44 glioma cells were cultured under neural stem cell medium and glioma stem cell spheres were collected. Immunocytochemistry was used to dectet the expression of CD133, nestin, A2B5, vimentin, VEGFR-2 and IDH R132H. Cell spheres were induced using serum-containing medium, and the expression of CD133, nestin, vimentin, GFAP, ß-III tubulin and GalC in the cell spheres were detected. The expression of CD133, nestin, VEGFR-2, GFAP, S-100 and CD34 in the intracranial xenograft tumor tissues was detected using immunohistochemistry. The pathological characteristics of orthotopic xenograft tumors generated from the SHG-44 glioma cells and SHG-44 glioma stem cell spheres were compared. RESULTS: SHG-44 glioma stem cell spheres were collected successfully after cultured under neural stem cell medium. The ratio of CD133(+) cells in the passage 10 SHG-44 glioma stem cell spheres was (71.63 ± 5.92)%, significantly higher than that in the SHG-44 glioma cells [(1.95 ± 1.45)%]. Immunocytochemistry showed that in the SHG-44 glioma cell spheres, the ratio of nestin(+) cells was (84.06 ± 7.58)%, vimentin(+) cells (29.11 ± 3.44)%, VEGFR 2(+) cells (64.44 ± 3.69)%, and A2B5(+) cells (14.08 ± 2.19)%. A subpopulation of cells with mutation of IDH R132H was detected harboring in the SHG-44 glioma cell spheres. After induction of differentiation with serum-containing medium, the ratio of CD133(+) cells was (1.89 ± 1.27)%, nestin(+) cells (6.67 ± 2.75)%, vimentin(+) cells (93.75 ± 2.95)%, GFAP (+) cells (91.33 ± 4.75)%, ß-III tubulin(+) cells (82.36 ± 4.02)%, and GalC(+) cells (8.92 ± 3.19)%. Immunohistochemistry showed positive expression of GFAP, S-100, VEGFR-2, and negative of CD133 and nestin in the orthotopic xenograft tumors. A very small amount of human-specific CD34 cells formed a tubular structure. Compared with the SHG-44 glioma cell-formed xenograft tumor, the SHG-44 glioma stem cell-formed xenograft tumor exhibited a higher local invasiveness. CONCLUSIONS: SHG-44 glioma cell spheres are successfully collected after cultured under neural stem cell medium. They belong to the CD133(+)A2B5(-) GSC subpopulation, highly expressing VEGFR-2, possess the ability of both self-renewal and multi-directional differentiation, and may participate in the formation of vasculogenic mimicry.


Assuntos
Neoplasias Encefálicas/patologia , Glioma/patologia , Células-Tronco Neoplásicas/patologia , Animais , Neoplasias Encefálicas/metabolismo , Linhagem Celular Tumoral , Células Cultivadas , Proteína Glial Fibrilar Ácida/metabolismo , Glioma/metabolismo , Humanos , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Nus , Invasividade Neoplásica , Transplante de Neoplasias , Células-Tronco Neoplásicas/metabolismo , Proteínas S100/metabolismo , Receptor 2 de Fatores de Crescimento do Endotélio Vascular/metabolismo
10.
Asian Pac J Cancer Prev ; 13(10): 5137-42, 2012.
Artigo em Inglês | MEDLINE | ID: mdl-23244124

RESUMO

UHRF2 is a member of the ubiquitin plant homeo domain RING finger family, which has been proven to be frequently up-regulated in colorectal cancer cells and play a role as an oncogene in breast cancer cells. However, the role of UHRF2 in glioma cells remains unclear. In this study, we performed real-time quantitative PCR on 32 pathologically confirmed glioma samples (grade I, 4 cases; grade II, 11 cases; grade III, 10 cases; and grade IV, 7 cases; according to the 2007 WHO classification system) and four glioma cell lines (A172, U251, U373, and U87). The expression of UHRF2 mRNA was significantly lower in the grade III and grade IV groups compared with the noncancerous brain tissue group, whereas its expression was high in A172, U251, and U373 glioma cell lines. An in vitro assay was performed to investigate the functions of UHRF2. Using a lentivirus-based RNA interference (RNAi) approach, we down-regulated UHRF2 expression in the U251 glioma cell line. This down- regulation led to the inhibition of cell proliferation, an increase in cell apoptosis, and a change of cell cycle distribution, in which S stage cells decreased and G2/M stage cells increased. Our results suggest that UHRF2 may be closely related to tumorigenesis and the development of gliomas.


Assuntos
Neoplasias Encefálicas/genética , Glioma/genética , RNA Mensageiro/genética , RNA Interferente Pequeno/genética , Ubiquitina-Proteína Ligases/genética , Adulto , Apoptose , Encéfalo/metabolismo , Neoplasias Encefálicas/metabolismo , Neoplasias Encefálicas/patologia , Ciclo Celular , Proliferação de Células , Feminino , Citometria de Fluxo , Seguimentos , Regulação Neoplásica da Expressão Gênica , Glioma/metabolismo , Glioma/patologia , Humanos , Técnicas In Vitro , Masculino , Gradação de Tumores , Prognóstico , Reação em Cadeia da Polimerase em Tempo Real , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Fatores de Risco , Células Tumorais Cultivadas , Ubiquitina-Proteína Ligases/antagonistas & inibidores , Ubiquitina-Proteína Ligases/metabolismo
11.
Anal Cell Pathol (Amst) ; 35(3): 167-78, 2012.
Artigo em Inglês | MEDLINE | ID: mdl-22155992

RESUMO

BACKGROUND: The gliomas represent the most common primary malignant brain tumors; however, little is known about the molecular pathogenesis of these tumors. Recent research reveals that the oncogenesis and development of gliomas have a close relation to the overexpression of several oncogenes and the inactivation of tumor suppressor genes. Whether the RING finger protein, RNF138, a newly discovered protein, plays a role in glioma oncogenesis is unknown. The present study investigates the expression levels of RNF138 mRNA in glioma samples and noncancerous brain samples and its function in the human glioma cell line U251. METHODS: RT-PCR was used to ascertain the expression of RNF138 mRNA in the glioma cell lines U251, SHG44, U87, A172, and U373. The RNF138 mRNA expression levels of 35 pathological confirmed glioma samples (Grade I - 4 cases, Grade II - 13 cases, Grade III - 11 cases, and Grade IV - 7 cases) and five noncancerous brain tissue samples were analyzed by real-time quantitative PCR. By RNA interference (RNAi) with the lentivirus vector system, the expression of RNF138 was inhibited in the human astrocytomas-glioblastoma multiforme cell line U251. The effects of RNF138-knockdown on cell proliferation were assessed by Cellomics, and cell cycle and cell apoptosis were assessed by FACS. RESULTS: The RNF138 mRNA is expressed in the five glioma cell lines, and its expression level is significantly higher in glioma tissue than in noncancerous brain tissue. By down-regulation of RNF138 expression, U251 cell proliferation was inhibited and cell apoptosis increased. At the same time, S stage cells lessened and G2 stage cells increased. CONCLUSION: The RNF138 gene is highly expressed in glioma tissue and glioma cell lines. It plays an important role in glioma cell proliferation, apoptosis, and cell cycle.


Assuntos
Neoplasias Encefálicas/genética , Regulação Neoplásica da Expressão Gênica/fisiologia , Glioma/genética , Domínios RING Finger/genética , Ubiquitina-Proteína Ligases/genética , Adulto , Apoptose , Neoplasias Encefálicas/metabolismo , Neoplasias Encefálicas/patologia , Ciclo Celular/fisiologia , Linhagem Celular Tumoral , Proliferação de Células , Feminino , Glioma/metabolismo , Glioma/patologia , Humanos , Masculino , Receptores de Superfície Celular/biossíntese , Receptores de Superfície Celular/genética
12.
J Exp Clin Cancer Res ; 30: 114, 2011 Dec 20.
Artigo em Inglês | MEDLINE | ID: mdl-22185393

RESUMO

BACKGROUND: Zfx is a zinc finger protein of the Zfy family, whose members are highly conserved in vertebrates. Zfx is a shared transcriptional regulator of both embryonic stem cells (ESC) and hematopoietic stem cells (HSC), which suggests a common genetic basis of self-renewal in embryonic and adult stem cells. The level of Zfx expression correlates with aggressiveness and severity in many cancer types, including prostate cancer, breast cancer, and leukemia. However, the importance of Zfx in human glioma is largely unknown. In the present study, we examined the role of Zfx in human glioma. METHODS: We detected expression levels of Zfx mRNA in U251 cells, U87 cells, U373 cells, and A172 cells by semi-quantitative RT-PCR. To analyze the expression of Zfx mRNA in glioma tissues, we performed real-time quantitative PCR on 35 pathologically confirmed glioma samples (Grade I-4cases, Grade II-13cases, Grade III-11cases, and Grade IV-7cases) and on 5 noncancerous brain tissue samples. We used lentivirus-mediated small interfering RNAs (siRNAs) to knock down Zfx expression in the human malignant glioma cell line U251. Changes in Zfx target gene expression were determined by real-time RT-PCR. Cell proliferation was examined by a High Content Screening assay. DNA synthesis in proliferating cells was determined by BrdU incorporation. Cell cycle distribution and apoptosis were detected by flowcytometric analysis. RESULTS: We discovered that Zfx mRNA was expressed in U251 cells, U87 cells, U373 cells, and A172 cells. The expression level of Zfx is significantly higher in gliomas compared to noncancerous brain tissue. Using a lentivirus-based RNAi approach, Zfx expression was significantly inhibited in human glioblastoma U251 cells. The effects of Zfx knockdown on cell proliferation, cell cycle distribution, and apoptosis were assessed. Inhibition of Zfx expression in U251 cells by RNAi significantly impaired cell proliferation, increased apoptosis, and arrested cells in S phase. CONCLUSIONS: The results of our study demonstrate that the Zfx gene is highly expressed in glioma tissue and in glioma cell lines. Furthermore, Zfx may play a critical role in cell proliferation, cell cycle distribution, and apoptosis of human malignant glioma cells.


Assuntos
Apoptose/genética , Neoplasias Encefálicas/genética , Neoplasias Encefálicas/patologia , Glioma/genética , Glioma/patologia , Fatores de Transcrição Kruppel-Like/genética , Dedos de Zinco/genética , Neoplasias Encefálicas/metabolismo , Processos de Crescimento Celular/genética , Linhagem Celular Tumoral , Glioma/metabolismo , Humanos , Fatores de Transcrição Kruppel-Like/biossíntese , RNA Mensageiro/biossíntese , RNA Mensageiro/genética
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