The HMGB1 Knockout SK-OV-3 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal population of SK-OV-3 human ovarian carcinoma cells with disruption of the target gene HMGB1. This gene-edited pool provides a loss-of-function model for studying the pleiotropic roles of HMGB1 in nuclear architecture and extracellular signaling. The polyclonal format ensures a heterogeneous collection of knockout alleles, enabling robust population-level analyses without clonal bias.
The parental SK-OV-3 cell line is derived from the ascites of a patient with ovarian adenocarcinoma and serves as a widely used model of high-grade serous ovarian cancer. These epithelial cells harbor mutant p53 and amplified HER2/neu, and exhibit an aneuploid karyotype, reflecting the genomic instability characteristic of advanced ovarian malignancies. SK-OV-3 cells are extensively employed in studies of ovarian cancer biology, chemoresistance, and metastasis.
HMGB1 encodes a conserved nuclear protein regulating DNA organization and repair. Extracellularly, as a DAMP, HMGB1 binds TLR4, RAGE, TLR2, and TREM1, stimulating the MyD88-IRAK-TRAF6 axis to activate NF-??B and MAPK1/3. This induces expression of TNF-??, IL-6, and MMP-9, promoting inflammation and migration. HMGB1 is controlled by TNF-??, IL-1??, LPS, p53, and HIF-1??, and interacts with CD24 and CXCL12.
In SK-OV-3 cells, HMGB1 is implicated in driving DAMP-mediated inflammation and tumor progression. The mutant p53 background may alter HMGB1-related DNA repair dynamics, while amplified HER2/neu could modulate downstream MAPK signaling. Ablation of HMGB1 in this line disrupts autocrine and paracrine inflammatory loops, potentially attenuating NF-??B-dependent gene expression and reducing migratory and invasive capacity. The knockout model thus provides a defined genetic background to dissect HMGB1??s contributions to ovarian cancer pathology, particularly in the context of chemoresistance and metastatic dissemination.
This polyclonal knockout pool is suited for a broad range of assays, including Western blotting and ELISA to monitor intracellular and secreted HMGB1 levels, RT-qPCR for downstream target genes, NF-??B luciferase reporter assays, immunofluorescence for subcellular localization, flow cytometry for RAGE expression, Transwell migration/invasion analysis, and Annexin V apoptosis assessment. Applications encompass investigation of DAMP-mediated inflammation in ovarian cancer, study of HMGB1??s role in chemoresistance and metastasis, evaluation of anti-inflammatory therapies targeting HMGB1, and analysis of autophagy-apoptosis crosstalk. For detailed product specifications or custom gene editing inquiries, please contact Ascent Research.
