The HMGB2 Knockout SK-HEP-1 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from the SK-HEP-1 human liver adenocarcinoma cell line, in which the high mobility group box 2 (HMGB2) gene has been disrupted. This polyclonal knockout model is generated by CRISPR/Cas9-mediated gene disruption, resulting in a heterogeneous mixture of cells carrying various loss-of-function edits in the HMGB2 locus, and is provided as a ready-to-use pooled population for functional studies without single-cell cloning.
The parental SK-HEP-1 cell line is a well-established epithelial adenocarcinoma model originally isolated from the ascites of a patient with liver cancer. These cells display characteristics of hepatocellular carcinoma (HCC) and serve as a valuable in vitro system for investigating molecular mechanisms of hepatic tumorigenesis, metastatic behavior, and therapeutic responses. The SK-HEP-1 background supports the study of HMGB2 in a context that recapitulates key aspects of liver cancer biology, including proliferative signaling, inflammatory crosstalk, and genomic instability.
HMGB2 functions both as a nuclear architectural factor that binds and bends DNA to regulate transcription, DNA repair, and chromatin organization, and as an extracellular damage-associated molecular pattern (DAMP) that triggers inflammation by engaging receptors such as RAGE and TLR4. In the nucleus, HMGB2 interacts with transcription complex proteins and modulates the expression of genes involved in cell cycle progression and survival. Under stress conditions, HMGB2 can be released into the extracellular space, where it activates NF-??B signaling through the MyD88?CIRAK?CIKK cascade, leading to p65 translocation and production of pro-inflammatory cytokines including IL-6 and IL-8. Its activity is regulated by upstream signals such as TNF-??, IL-1??, LPS, and oxidative stress, and it is also transcriptionally controlled by p53. Downstream, HMGB2 promotes expression of NF-??B, IL-6, IL-8, MMP9, cyclin D1, and Bcl-2, thereby linking inflammation, survival, and proliferation pathways.
Knockout of HMGB2 in SK-HEP-1 cells eliminates its dual role in chromatin modulation and extracellular inflammatory signaling, providing a clean loss-of-function model to dissect its contribution to HCC-associated processes. Disruption of HMGB2 is expected to impair NF-??B and RAGE-mediated signaling, reduce cytokine production, and compromise DNA repair and transcriptional programs that support tumor cell survival and invasiveness. This model is particularly suited for evaluating HMGB2 as a therapeutic target in hepatocellular carcinoma and for exploring its involvement in inflammation-driven cancer progression, senescence bypass, and fibrosis-associated signaling networks.
Researchers can use this polyclonal knockout population in a wide range of functional assays to investigate the mechanistic roles of HMGB2. Representative applications include western blotting and RT-qPCR to confirm HMGB2 loss, NF-??B luciferase reporter assays to measure transcriptional activity, and ELISA to quantify IL-6 and IL-8 production. Additional phenotypic analyses such as MTT-based proliferation assays and Transwell migration/invasion assays can assess the impact on tumor cell behavior. Transcriptome profiling via RNA-seq and chromatin occupancy analysis by ChIP-qPCR further enable global and locus-specific insights into HMGB2-dependent gene regulation. For further information or inquiries about this product, please contact Ascent Research.
