| Field | Specification |
|---|---|
| Mfr No | |
| Species |
LN229 is a human glioblastoma cell line derived from a 60-year-old White female patient with glioblastoma multiforme (GBM), specifically from the right frontal parieto-occipital cortex. Glioblastoma is one of the most aggressive and lethal forms of brain cancer, and LN229 cells are extensively used in research to understand the disease's molecular underpinnings and to develop potential therapeutic strategies. The cells display an epithelial-like morphology and exhibit adherent growth properties, which makes them ideal for in vitro studies. Given their high tumorigenic potential, they readily form tumors when injected into nude mice, making them a robust model for cancer research.
One of the critical characteristics of LN229 cells is the presence of a mutated p53 gene (TP53), with a specific CCT (Pro) to CTT (Leu) mutation at codon 98. This mutation contributes significantly to the cell line's aggressive behavior and resistance to apoptosis. Additionally, LN229 cells have a wild-type PTEN gene, but they exhibit homozygous deletions in the p16 and p14ARF tumor suppressor genes, which are vital regulators of the cell cycle and apoptosis. These genetic alterations make LN229 a valuable model for studying the impact of these mutations on tumor biology and therapeutic resistance.
LN229 cells are particularly useful in apoptosis studies. They undergo apoptosis upon stimulation with Fas ligand, with cell death occurring within 16 hours. Interestingly, while Bcl-2 expression can protect LN229 cells from Fas ligand-induced apoptosis, it only offers limited protection against apoptosis induced by puromycin, a protein synthesis inhibitor. This selective resistance pattern makes LN229 cells a critical model for understanding the molecular mechanisms of apoptosis in glioblastoma and for testing potential apoptosis-modulating therapies. As with all in vitro research models, LN229 cells are not suitable for therapeutic or in vivo applications.
—
- cultureMedium: DMEM, w: 4.5 g/L Glucose, w: 4 mM L-Glutamine, w: 3.7 g/L NaHCO3, w: 1.0 mM Sodium pyruvate (Cytion article number 820300a)
- supplements: Supplement the medium with 10% FBS
- dissociationReagent: Accutase
- doublingTime: 31 hours
- subculturing: Remove the old medium from the adherent cells and wash them with PBS that lacks calcium and magnesium. For T25 flasks, use 3-5 ml of PBS, and for T75 flasks, use 5-10 ml. Then, cover the cells completely with Accutase, using 1-2 ml for T25 flasks and 2.5 ml for T75 flasks. Let the cells incubate at room temperature for 8-10 minutes to detach them. After incubation, gently mix the cells with 10 ml of medium to resuspend them, then centrifuge at 300xg for 3 minutes. Discard the supernatant, resuspend the cells in fresh medium, and transfer them into new flasks that already contain fresh medium.
- fluidRenewal: 2 to 3 times per week
- freezeMedium: As a cryopreservation medium, use complete growth medium (including FBS) + 10% DMSO for adequate post-thaw viability, or CM-1 (Cytion catalog number 800100), which includes optimized osmoprotectants and metabolic stabilizers to enhance recovery and reduce cryo-induced stress.
- On the influence of cannabinoids on cell morphology and motility of glioblastoma cells
- Jamming Transitions in Astrocytes and Glioblastoma Are Induced by Cell Density and Tension
- An optimized protocol for metabolic measurement in 3D tumor spheroids derived from primary and established glioblastoma cells
- Nimodipine Used with Vincristine: Protects Schwann Cells and Neuronal Cells from Vincristine-Induced Cell Death but Increases Tumor Cell Susceptibility
- Synthetic Cannabinoids Influence the Invasion of Glioblastoma Cell Lines in a Cell- and Receptor-Dependent Manner
- IDH1(R132H) mutation causes a less aggressive phenotype and radiosensitizes human malignant glioma cells independent of the oxygenation status.
- Histone deacetylase inhibitors promote glioma cell death by G2 checkpoint abrogation leading to mitotic catastrophe
- Betulinic Acid Derivatives NVX-207 and B10 for Treatment of Glioblastoma—An in Vitro Study of Cytotoxicity and Radiosensitization
- Integrative analysis of therapy resistance and transcriptomic profiling data in glioblastoma cells identifies sensitization vulnerabilities for combined modality radiochemotherapy
- Nimodipine Used with Vincristine: Protects Schwann Cells and Neuronal Cells from Vincristine-Induced Cell Death but Increases Tumor Cell Susceptibility.
- Localization matters: nuclear-trapped Survivin sensitizes glioblastoma cells to temozolomide by elevating cellular senescence and impairing homologous recombination
- Class I HDAC overexpression promotes temozolomide resistance in glioma cells by regulating RAD18 expression
- XRCC3 contributes to temozolomide resistance of glioblastoma cells by promoting DNA double-strand break repair.
- Evaluation of the Betulinic Acid-Cisplatin conjugate APC and its precursor DE9B for the treatment of human malignant glioma.
- Systematic in vitro analysis of therapy resistance in glioblastoma cell lines by integration of clonogenic survival data with multi-level molecular data
- The influence of biomechanical properties and cannabinoids on tumor invasion.
- Targeting Homologous Recombination by Pharmacological Inhibitors Enhances the Killing Response of Glioblastoma Cells Treated with Alkylating Drugs
10%
OFF
15%OFF
20%
OFF
$50
OFF
FREE
SAMPLE
