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GOS-3
Cat.No.: CSC-C0452
Species: Human
Source: glioblastoma
Morphology: fibroblastoid, adherent cells growing as monolayer
Culture Properties: monolayer
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Immunology: cytokeratin -, desmin -, endothel -, GFAP +, neurofilament -, vimentin +
Viruses: ELISA: rev
The GOS-3 cell line was originally described as a glioma cell line established from brain tumor material of a 55-year-old male with mixed astrocytoma (grade II/III). Subsequent short tandem repeat (STR) analysis revealed that the GOS-3 cells are actually derived from the human glioblastoma cell line U-343-MG. These cells are extensively employed in scientific research to model the biological characteristics of human glioblastoma. Morphologically, GOS-3 cells exhibit a fibroblast-like appearance, characterized by a distinctive spindle shape, oval nuclei, rich cytoplasm, and growth as an adherent monolayer. In terms of molecular expression, the GOS-3 cell line expresses various specific proteins, including glial fibrillary acidic protein (GFAP), vimentin, S-100 protein, pp60C-SRC, ciliary neurotrophic factor (CNTF), leukemia inhibitory factor (LIF), and their receptors. Notably, experimental results show that LIF and oncostatin M in this cell line can inhibit cell growth and differentiation, indicating their critical role in regulating cellular proliferation and differentiation.
Given their glioma origin, researchers can exploit the GOS-3 cell line to investigate the mechanisms underlying glioma growth, invasion, and metastasis, as well as to explore potential therapeutic targets. Additionally, this cell line is suited for screening compounds with anti-tumor activity, assisting in the development of novel therapeutic strategies. The GOS-3 cell line also serves as a model for examining fundamental biological processes such as cell proliferation, differentiation, apoptosis, and signal transduction.
ALDH5A1 Gene Knockdown Reduces Glioblastoma Cell Viability
Gliomas are the most common primary malignant brain tumors. Metabolic reprogramming, specifically the dysregulation of aldehyde dehydrogenase (ALDH) enzymes, plays a significant role in glioma progression. Piperi et al. focuses on the biological role and clinical significance of ALDH5A1, a less-studied ALDH family member, in diffuse gliomas. To investigate ALDH5A1's role in glioma progression, they knocked down ALDH5A1 using siRNA in high-expressing glioblastoma cell lines GOS-3 and SJ-GBM2. Post-48-hour transfection, western blot analysis confirmed ALDH5A1 silencing, showing a 61% reduction in SJ-GBM2 and 49% in GOS-3 cells (Fig. 1A). XTT assays at 24 hours revealed decreased cell viability in siALDH5A1-transfected cells compared to controls, with a reduction of 53.1% in SJ-GBM2 and 38.2% in GOS-3 (Fig. 1B). BAX mRNA levels increased but were not statistically significant (Fig. 1C). Enhanced caspase-3 cleavage was observed in both cell lines after ALDH5A1 knockdown (Fig. 1D). These findings indicate that ALDH5A1 down-regulation reduces glioma cell viability and induces apoptotic pathways.
Fig. 1. Glioblastoma cells exhibit reduced cell proliferation following siALDH5A1 transfection, increased BAX mRNA levels and induced caspase-3 cleavage (Piperi, C., Saurty-Seerunghen, M. S., et al., 2023).
PCDHB4 Inhibits Cell Proliferation and Migration
Aberrant DNA methylation critically regulates gene expression in glioblastoma (GBM), yet its effect on PCDHB4 in GBM is unclear. Huang et al. discovered a novel methylation-driven gene PCDHB4 for the diagnosis and prognosis of GBM and demonstrated that PCDHB4 is a tumor suppressor in vitro experiments. The qRT-PCR results showed that PCDHB4 mRNA expression was significantly lower in GBM tumor tissue compared to adjacent normal tissue (Fig. 2A). Further, treating hypermethylated GOS3 and U87MG cell lines with 5-Aza increased PCDHB4 mRNA expression, peaking at 1 µM and 2 µM concentrations respectively (Fig. 2B and C). To investigate PCDHB4's role as a methylation-driven gene in GBM, they correlated PCDHB4's methylation with mRNA expression in GOS3 and U87MG cell lines. They constructed and verified PCDHB4 overexpression plasmids and analyzed cell proliferation and vitality (Fig. 2D and E). Overexpression of PCDHB4 reduced cell proliferation and vitality, as shown in CCK8 (Fig. 2F and G) and EdU assays (Fig. 3A and B). Additionally, wound healing assays indicated significantly reduced migration capabilities in PCDHB4 over-expressing cells (Fig. 3C and D). These findings suggest PCDHB4 inhibits GBM progression.
Fig. 2. PCDHB4 downregulated in glioma tissues and increased with demethylation (Huang, H., Xie, Y., et al., 2023).
Fig. 3. PCDHB4 inhibits cell proliferation and migration (Huang, H., Xie, Y., et al., 2023).
Collect the cells by centrifugation, remove the supernatant thoroughly from the centrifuge tube, add the appropriate amount of serum-free cell lyophilisation solution to the tube to make a cell lyophilisation suspension and place in a -80°C refrigerator for long-term freezing or transfer to liquid nitrogen
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This product is ideal for studying cell migration due to cell-cell interaction with the extracellular matrix.
05 Oct 2021
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Description: Established from the surgical resection of a left parieto-occipital glioblastoma from a 47-year-old man in 1980; cells were described to secrete plasminogen activator, to be clonogenic in soft agar and to be tumorigenic in nude mice; DNA fingerprinting showed unequivocally that SNB-19 is a subclone of the astrocytoma cell line U-251 MG)
