Publications by authors named "Sheng-Hua Chu"

Gliomas are the most common primary brain tumours, and glioblastomas (GBMs) are subgrouped into four distinct molecular subtypes. This study aimed to identify the potential gene related to glioma progression. Weighted gene co-expression network analysis (WGCNA) was used to explore the related gene.

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Meningiomas are the most common primary intracranial tumor in adults. However, to date, systemic coexpression analyses for meningiomas fail to explain its pathogenesis. The aim of the present study was to construct coexpression modules and identify potential biomarkers associated with meningioma progression.

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Gliomas are the most prevalent malignant primary brain tumors with poor outcome, and four different molecular subtypes (Mesenchymal, Proneural, Neural, and Classical) are popularly applied in scientific researches and clinics of gliomas. Public databases contain an abundant genome-wide resource to explore the potential biomarker and molecular mechanisms using the informatics analysis. The aim of this study was to discover the potential biomarker and investigate its effect in gliomas.

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Ependymomas (EPNs) are one of the most common types of malignant neuroepithelial tumors. In an effort to identify potential biomarkers involved in the pathogenesis of EPN, the mRNA expression profiles of the GSE25604, GSE50161, GSE66354, GSE74195 and GSE86574 datasets, in addition to the microRNA (miRNA/miR) expression profiles of GSE42657 were downloaded from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) and differentially expressed miRNAs (DEMs) between EPN and normal brain tissue samples were identified using the Limma package in R and GEO2R, respectively.

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Article Synopsis
  • Medulloblastoma (MB) is the most common type of harmful brain tumor in kids, and this study aims to find important markers that can help understand it better.
  • Researchers analyzed data from different gene studies and found 1,006 genes that were either increased or decreased in MB compared to normal samples.
  • They identified key genes that might affect how MB develops and how patients might survive, which can lead to new treatments for this type of cancer.
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Glioblastoma multiforme (GBM) is the most common malignant tumor of the central nervous system and has a very poor prognosis. Currently, patients were treated by resection followed by radiotherapy plus concurrent temozolomide (TMZ) chemotherapy. However, many patients are resistant to TMZ-induced DNA damage because of upregulated expression of the DNA repair enzyme O-methylguanine-DNA methyltransferase (MGMT).

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Background: Anti-angiogenic therapy inhibits tumor growth and is considered as a potential clinical therapy for malignant glioma. However, inevitable recurrences and unexpected tumor resistance, particularly increased invasion ability of glioma cell, were observed after anti-angiogenic treatment. The underlying mechanism remains undetermined.

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Special AT-rich sequence-binding protein-1 (SATB1) has been reported to be over-expressed in many human tumors and knockdown of SATB1 can inhibit tumor growth. The present study was designed to determine the role of SATB1 in the growth of human glioma U251 cells using the plasmid-based SATB1 short hairpin RNA (shRNA) delivered by hydroxyapatite nanoparticles in vitro and in vivo. The in vitro growth, invasion and angiogenesis assays of human glioma U251 cells were done.

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Background: Previous study showed that hydroxyapatite nanoparticles (nano-HAPs) inhibited glioma growth in vitro and in vivo; and in a drug combination, they could reduce adverse reactions. We investigated the possible enhancement of radiosensitivity induced by nano-HAPs.

Methods: In vitro radiosensitization of nano-HAPs was measured using a clonogenic survival assay in human glioblastoma U251 and breast tumor brain metastatic tumor MDA-MB-231BR cells.

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Background: Our previous study showed that SLC22A18 downregulation and promoter methylation were associated with the development and progression of glioma and the elevated expression of SLC22A18 was found to increase the sensitivity of glioma U251 cells to the anticancer drug 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU). In this study, we investigated the predictive value of SLC22A18 promoter methylation and protein expression in glioblastoma multiforme (GBM) patients receiving temozolomide (TMZ) therapy.

Patients And Methods: SLC22A18 promoter methylation and protein expression were examined by methylation-specific polymerase chain reaction (MSP) and Western blotting respectively, then we compared SLC22A18 promoter methylation and protein expression in tumor cell explants in regard to prediction of TMZ response and survival time of 86 GBM patients.

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Special AT-rich-sequence-binding protein 1 (SATB1), a new type of gene regulator, has been reported to be expressed in various human cancers and may be associated with malignancy. The aim of this study was to investigate the expression of SATB1 in astrocytoma and to determine its prognostic value for the overall survival of patients with astrocytoma. The expression of SATB1 protein and messenger RNA (mRNA) in human astrocytoma specimens was examined using immunohistochemistry and semi-quantitative reverse transcription polymerase chain reaction (RT-PCR).

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Special AT-rich sequence-binding protein-1 (SATB1) has been reported to be overexpressed in numerous human tumors. The aim of the present study was to determine the correlation and clinical significance between the expression of SATB1 and B-cell lymphoma 2 (Bcl-2) in human glioblastoma multiforme (GBM). Samples from 70 patients with GBMs were analyzed and 10 normal brain tissues were used as the control group.

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Hydroxyapatite nanoparticles (nano-HAPs) have been reported to exhibit antitumor effects on various human cancers, but the effects of nano-HAPs on human glioma cells remain unclear. The aim of this study was to explore the inhibitory effect of nano-HAPs on the growth of human glioma U251 and SHG44 cells in vitro and in vivo. Nano-HAPs could inhibit the growth of U251 and SHG44 cells in a dose- and time-dependent manner, according to methyl thiazoletetrazolium assay and flow cytometry.

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Previous studies showed that solute carrier family 22 member 18 (SLC22A18) is involved in tumorigenesis. The aim of this study was to examine the role of SLC22A18 in glioma cells. Glioma U251 cells were transfected with the human SLC22A18 gene.

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Article Synopsis
  • The study investigates the role of SATB1, a protein linked to various human cancers, in gliomas, focusing on its expression levels, associations with cancer aggressiveness, and potential impacts on patient survival.
  • Researchers found that SATB1 was expressed in 62.9% of glioma tumors and correlated with higher tumor grades, increased cell proliferation (Ki67), and poorer patient outcomes, while showing an inverse relationship with MGMT promoter methylation.
  • In laboratory tests, reducing SATB1 expression in U251 glioma cells led to decreased growth, invasion, and new blood vessel formation, while promoting cell death, suggesting SATB1 might be a crucial factor in glioma progression and a potential target for therapy.
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We investigated the expression of the putative tumor suppressor SLC22A18 to evaluate it as a prognostic marker in glioma patients. Immunohistochemical and Western blot analyses of clinical tissue samples obtained from 120 patients with glioma were performed. Low expression of SLC22A18 was observed in 71.

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SLC22A18 [solute carrier family 22 (organic cation transporter) member 18] is located within the 11p15.5 cluster, and may be a new tumor suppressor gene; evidence of SLC22A18 hypermethylation is documented in several types of human cancers. In order to determine whether SLC22A18 hypermethylation is involved in glioma, we determined the SLC22A18 gene protein expression, mRNA expression and methylation status in glioma U251 cells before and after treatment with 5-Aza-2'‑deoxycytidine (5-Aza-CdR), and observed the change in growth.

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Background: Downregulation of the putative tumor suppressor gene SLC22A18 has been reported in a number of human cancers. The aim of this study was to investigate the relationship between SLC22A18 downregulation, promoter methylation and the development and progression of human glioma.

Method: SLC22A18 expression and promoter methylation was examined in human gliomas and the adjacent normal tissues.

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The hepatocyte growth factor (HGF) and vascular endothelial growth factor (VEGF) are important cytokines with modulatory actions in the nervous system. The present study aimed to investigate the role and expression of HGF and VEGF in the cerebral tissue of adult rats with chronic hydrocephalus after subarachnoid hemorrhage. Adult female Wistar rats were randomly divided into 4 groups: a control group (n=20) and 3 experimental subgroups (n=60).

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Cell culture, tissue chemistry and flow cytometry were used to determine whether antisense c-Met oligodeoxynucleotides enhanced the sensitivity of human glioma cells to paclitaxel. A combination of paclitaxel with antisense c-Met oligodeoxynucleotides inhibited cell growth, induced apoptosis and induced c-Met protein expression in U251 and SHG44 human glioma cells more significantly than either paclitaxel or the oligodeoxynucleotides on their own (P<0.01).

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Epidermoid cysts are uncommon, benign and slow-growing lesions. They often reach an enormous size without producing neurologic symptoms. We describe a 35-year-old female who had a giant intradiploic epidermoid cyst of the occipital bone.

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Article Synopsis
  • * The study utilized RNA interference (RNAi) to create shRNA vectors specifically targeting the c-Met gene in glioma U251 cells, significantly reducing c-Met expression by up to 90%.
  • * Results showed that inhibiting c-Met led to decreased growth and metastasis of U251 cells and increased apoptosis, suggesting RNAi targeting of c-Met could be an effective strategy for antiangiogenic cancer therapies.
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Hypoxia regulates expression of hepatocyte growth factor (HGF) by increasing its transcription and by stabilizing its mRNA. Despite the pivotal role of hypoxia-inducible factor 1 (HIF-1) in transcriptional activation of hypoxia-responsive genes, it is not known whether HIF-1 mediates hypoxia-induced stabilization of HGF mRNA. We constructed adenoviral vectors expressing either the wild-type HIF-1alpha (Ad2/HIF-1alpha/FL), a constitutively stable hybrid form of HIF-1alpha (Ad2/HIF-1alpha/VP16), or no transgene (Ad2/CMVEV).

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Article Synopsis
  • Postoperative radiotherapy is the usual treatment for patients with a type of brain tumor called malignant glioma, but these tumors often come back because they resist radiation.
  • The study looked at how three different glioma cell lines reacted to radiation and measured a special protein called HGF, which is linked to tumor growth and survival.
  • The results showed that higher radiation doses increased HGF levels in all cell lines, but one specific cell line (BT325) had much more HGF and was harder to kill with radiation, suggesting it could grow back even after treatment.
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