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Cancer: Astrocytoma
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Total 35 results found since Jan 2013.
Galectin-3 Mediates Tumor Progression in Astrocytoma by Regulating Glycogen Synthase Kinase-3 β Activity
This study aims to validate the correlation between the clinical outcomes and protein expression of galectin-3/GSK3B in astrocytoma. Immunohistochemistry staining was performed to detect galectin-3/GSK3B protein expression in patients with astrocytoma. The Chi-square test, Kaplan-Meier evaluation, and Cox regression analysis were used to determine the correlation between clinical parameters and galectin-3/GSK3B expression. Cell proliferation, invasion, and migration were compared between a non-siRNA group and a galectin-3/GSK3B siRNA group. Protein expression in galectin-3 or GSK3B siRNA-treated cells was evaluated using w...
Source: Current Issues in Molecular Biology - May 15, 2023 Category: Molecular Biology Authors: Hung-Pei Tsai Chien-Ju Lin Ann-Shung Lieu Yi-Ting Chen Tzu-Ting Tseng Aij-Lie Kwan Joon-Khim Loh Source Type: research
Viruses, Vol. 15, Pages 97: HLA-A, HSPA5, IGFBP5 and PSMA2 Are Restriction Factors for Zika Virus Growth in Astrocytic Cells
Conclusions: The top ZIKV dysregulated cellular networks were antimicrobial response, cell death, and energy production while top dysregulated functions were antigen presentation, viral replication and cytopathic impact. Th1 and interferon signaling pathways were among the top dysregulated canonical pathways. siRNA-mediated KD of HLA-A, IGFBP5, PSMA2 and HSPA5 increased ZIKV titers and protein synthesis, indicating they are ZIKV restriction factors. ZIKV infection also restored HLA-A expression in HLA-A KD cells by 48 h post-infection, suggesting interactions between this gene product and ZIKV.
Source: Viruses - December 29, 2022 Category: Virology Authors: Affan A. Sher Ying Tenny Lao Kevin M. Coombs Tags: Article Source Type: research
Distinct expression and function of breast cancer metastasis suppressor 1 in mutant P53 glioblastoma
ConclusionOur data indicate upregulation of BRMS1 in high grade astrocytomas which correlates positively withmutant P53 and a poor patient survival. Silencing of BRMS1 inmutant P53 GBM cell lines resulted in a reduced cellular growth and migration/invasion by suppressing the EGFR-AKT/NF-kB signaling pathway. BRMS1 may serve as a predictive biomarker and therapeutic target inmutant P53 GBM.
Source: Cellular Oncology - October 26, 2022 Category: Cancer & Oncology Source Type: research
MicroRNA-640 Inhibition Enhances the Chemosensitivity of Human Glioblastoma Cells to Temozolomide by Targeting Bcl2 Modifying Factor
Biochem Genet. 2022 Aug 19. doi: 10.1007/s10528-022-10264-x. Online ahead of print.ABSTRACTGlioblastoma (GBM) is the most malignant and challenging type of astrocytoma and also notoriously acknowledged as the most common primary brain tumor globally. Currently, chemotherapy is the most master therapy for tumor and is essential in clinical treatment for GBM. Nevertheless, the characterization of chemotherapy resistance seriously hinders clinical chemotherapy treatment. Accordingly, there are imperious demands for the exploitation of novel chemosensitizer to promote the efficacy of chemotherapy. Our current study was conduct...
Source: Biochemical Genetics - August 19, 2022 Category: Genetics & Stem Cells Authors: Shu Jiang Chao Luo Yongli Chen Jing Chen Shuang Tao Quan Zou Chunzhi He Shanwu Dong Source Type: research
Viruses, Vol. 13, Pages 1533: Inhibitors of Venezuelan Equine Encephalitis Virus Identified Based on Host Interaction Partners of Viral Non-Structural Protein 3
In this study, we utilized an overexpression construct encoding HA-tagged nsP3 to identify host proteins that interact with VEEV nsP3 by mass spectrometry. Bioinformatic analyses of the putative interactors identified 42 small molecules with the potential to inhibit the host interaction targets, and thus potentially inhibit VEEV. Three inhibitors, tomatidine, citalopram HBr, and Z-VEID-FMK, reduced replication of both the TC-83 strain and the Trinidad donkey (TrD) strain of VEEV by at least 10-fold in astrocytoma, astroglial, and microglial cells. Further, these inhibitors reduced replication of the related New World (NW) ...
Source: Viruses - August 3, 2021 Category: Virology Authors: Allison Bakovic Nishank Bhalla Farhang Alem Catherine Campbell Weidong Zhou Aarthi Narayanan Tags: Article Source Type: research
LY294002 and sorafenib as inhibitors of intracellular survival pathways in the elimination of human glioma cells by programmed cell death
Cell Tissue Res. 2021 Jul 8. doi: 10.1007/s00441-021-03481-0. Online ahead of print.ABSTRACTGliomas are aggressive brain tumors with very high resistance to chemotherapy throughout the overexpression of multiple intracellular survival pathways. Therefore, the aim of the present study was to investigate for the first time the anticancer activity of LY294002, phosphatidylinositol 3-kinase (PI3K) inhibitor and sorafenib, and rapidly accelerated fibrosarcoma kinase (Raf) inhibitor in the elimination of human glioma cells by programmed cell death. MOGGCCM (anaplastic astrocytoma, III) and T98G (glioblastoma multiforme, IV) cell...
Source: Cell Research - July 8, 2021 Category: Cytology Authors: Zaj ąc A Sumorek-Wiadro J Maciejczyk A Langner E Wertel I Rzeski W Jakubowicz-Gil J Source Type: research
TRPM7 Induces Tumorigenesis and Stemness Through Notch Activation in Glioma
In this study, we determined the major contributor(s) to TRPM7 mediated glioma stemness by further deciphering each individual Notch signaling. We first determined whether TRPM7 is an oncotarget in glioblastoma multiforme (GBM) using the Oncomine database. Next, we determined whether TRPM7 silencing by siRNA TRPM7 (siTRPM7) induces cell growth arrest or apoptosis to reduce glioma cell proliferation using cell cycle analysis and annexin V staining assay. We then examined the correlations between the expression of TRPM7 and Notch signaling activity as well as the expression of GSC markers CD133 and ALDH1 in GBM by downregula...
Source: Frontiers in Pharmacology - December 14, 2020 Category: Drugs & Pharmacology Source Type: research
