The GPNMB Knockout SK-OV-3 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the human ovarian adenocarcinoma cell line SK-OV-3. This product features targeted disruption of the GPNMB gene, which encodes glycoprotein nmb, a transmembrane glycoprotein implicated in tumor progression. The use of CRISPR/Cas9 genome editing introduces knockout alleles across the cell population, generating a heterogeneous pool of GPNMB loss-of-function variants. This polyclonal format enables the study of gene function without clonal selection bias, making it suitable for capturing a broad range of phenotypic outcomes in ovarian cancer research.
The host cell line, SK-OV-3, is a well-characterized human ovarian adenocarcinoma model, derived from the ascites fluid of a 64-year-old female patient. It exhibits an epithelial morphology, a hypodiploid karyotype, and tumorigenic potential in vivo. SK-OV-3 cells are known to express relevant ovarian cancer biomarkers and respond to hormonal and growth factor stimuli, making them a robust system for ovarian cancer research and drug development.
GPNMB functions as a type I transmembrane glycoprotein that participates in cell adhesion, migration, and differentiation through interactions with integrins ??v??3 and ??5??1, as well as with CD44 and heparan sulfate proteoglycans (HSPGs). GPNMB is transcriptionally upregulated by MITF and is activated by TGF-??, Wnt ligands, and inflammatory cytokines such as IL-6. Downstream, GPNMB promotes the expression of Snail and Vimentin, and enhances the activity of matrix metalloproteinases MMP-2 and MMP-9. Mechanistically, GPNMB signaling converges on the PI3K/Akt/mTOR and Wnt/??-catenin pathways, while also intersecting with the MAPK/ERK and TGF-??/Smad cascades, driving tumor cell proliferation, invasion, and immune evasion.
In the SK-OV-3 ovarian cancer context, disruption of GPNMB provides a powerful tool to dissect its contributions to ovarian adenocarcinoma progression. GPNMB is frequently overexpressed in ovarian tumors and is associated with poor prognosis and metastatic spread. The polyclonal knockout model allows researchers to evaluate the collective impact of GPNMB loss on adhesion-dependent signaling, anoikis resistance, and cytoskeletal reorganization. By comparing the knockout population to wild-type SK-OV-3 cells, investigators can identify GPNMB-dependent alterations in cell morphology, colony formation, and response to chemotherapeutic agents, generating insights into its role as a potential therapeutic target.
This product is ideally suited for studies on ovarian cancer cell adhesion and migration, tumor invasion and metastasis, and immune modulation. Typical assays include Western blotting and RT-qPCR for gene and protein expression analysis, wound healing and transwell assays to measure motility and invasiveness, immunofluorescence and flow cytometry for phenotypic characterization, and co-immunoprecipitation for interaction studies. Phospho-signaling analysis and apoptosis assays enable evaluation of downstream pathway alterations and cell death responses, while drug sensitivity testing can assess GPNMB’s role in chemoresistance. For more information, please contact Ascent Research.
