Objective: To investigate the effects of isoliquiritigenin on the migration and invasion of human glioma stem cells and the underlying mechanism.
Methods: The stem cell markers CD133 and Nestin in SHG44 human glioma stem cells were examined with immunofluorescence microscopy. The migration and invasion ability of glioma stem cells was determined by transwell method. The mRNA and protein expression of matrix metalloproteinase (MMP)-2 and MMP-9 were detected by real-time RT-PCR and Western blot, respectively.
Results: CD133 and Nestin were positive in SHG44 cells. The number of migrated cells in SHG44 cells treated with 20 and 80 μmol/L isoliquiritigenin for 48 h were significantly lower than that in control group (76±5 and 42±4 vs. 85±6, all <0.01), and the number of migrated cells in 80 μmol/L isoliquiritigenin group was lower than that in 20 μmol/L isoliquiritigenin group (<0.01). The numbers of cells crossing through membrane in 20 and 80 μmol/L isoliquiritigenin groups were 190±13 and 130±9, respectively, which were significantly lower than that in control group (230±14, all <0.01), and the number of crossed cells in the 80 μmol/L isoliquiritigenin group was lower than that in 20 μmol/L isoliquiritigenin group (<0.01). The mRNA and protein expression levels of MMP-2 and MMP-9 were decreased compared with control group (<0.05 or <0.01), and the expression levels in 80 μmol/L isoliquiritigenin group were lower than those in 20 μmol/L isoliquiritigenin group (<0.05 or <0.01).
Conclusions: Isoliquiritigenin exhibits antitumor effects on glioma stem cells by inhibiting cell migration and invasion, which may be related to the down-regulation of MMP-2 and MMP-9.
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http://dx.doi.org/10.3785/j.issn.1008-9292.2018.04.12 | DOI Listing |
Cancers (Basel)
December 2024
Hugo W. Moser Research Institute at Kennedy Krieger, Baltimore, MD 21205, USA.
: CSCs are critical drivers of the tumor and stem cell phenotypes of glioblastoma (GBM) cells. Chromatin modifications play a fundamental role in driving a GBM CSC phenotype. The goal of this study is to further our understanding of how stem cell-driving events control changes in chromatin architecture that contribute to the tumor-propagating phenotype of GBM.
View Article and Find Full Text PDFJ Oral Rehabil
January 2025
Stomatology Hospital, School of Stomatology, Zhejiang University School of Medicine, Zhejiang Provincial Clinical Research Center for Oral Diseases of Zhejiang Province, Key Laboratory of Oral Biomedical Research of Zhejiang Province, Cancer Center of Zhejiang University, Engineering Research Center of Oral Biomaterials and Devices of Zhejiang Province, Hangzhou, China.
Objective: This review summarises the role of Gli1 (Glioma-associated oncogene homologue 1) mesenchymal stem cells in craniofacial growth and development or tissue repair, and their application in the treatment of some diseases.
Design: The search for this narrative review was conducted in PubMed and Web of Science using relevant keywords, including checking reference lists of journal articles by hand searching.
Results: Gli1 mesenchymal stem cells play an important role in the growth and development of the skull, tooth, periodontium and mandibular condyle.
Cancer Med
January 2025
Faculty of Medical Sciences, Neuroscience Research Center, Lebanese University, Hadath, Lebanon.
Background: Glioblastoma (GBM) is the most common primary brain tumor in adults and has a median survival of less than 15 months. Advancements in the field of epigenetics have expanded our understanding of cancer biology and helped explain the molecular heterogeneity of these tumors. B-cell-specific Moloney murine leukemia virus insertion site-1 (Bmi-1) is a member of the highly conserved polycomb group (PcG) protein family that acts as a transcriptional repressor of multiple genes, including those that determine cell proliferation and differentiation.
View Article and Find Full Text PDFPurpose: In glioblastoma, the therapeutically intractable and resistant phenotypes can be derived from glioma stem cells, which often have different underlying mechanisms from non-stem glioma cells. Aberrant signaling across the EGFR-PTEN-AKT-mTOR pathways have been shown as common drivers of glioblastoma. Revealing the inter and intra-cellular heterogeneity within glioma stem cell populations in relations to signaling patterns through these pathways may be key to precision diagnostic and therapeutic targeting of these cells.
View Article and Find Full Text PDFCurr Neurol Neurosci Rep
January 2025
Department of Neurosurgery, Gui de Chauliac Hospital, Montpellier University Medical Center, 80 Avenue Augustin Fliche, Montpellier, 34295, France.
Purpose Of Review: In low-grade glioma (LGG), besides the patient's neurological status and tumor characteristics on neuroimaging, current treatment guidelines mainly rely on the glioma's genetics at diagnosis to define therapeutic strategy, usually starting with surgical resection. However, this snapshot in time does not take into account the antecedent period of tumor progression and its interactions with the brain before presentation. This article reviews new concepts that pertain to reconstruct the history of previous interplay between the LGG's course and adaptive changes in the connectome within which the glioma is embedded over the years preceding the diagnosis.
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