The CAV2 Knockout MES-OV Polyclonal Cells represent a CRISPR/Cas9-mediated gene-disrupted polyclonal cell population generated through targeted inactivation of the human CAV2 gene in the MES-OV ovarian endometrioid carcinoma cell line. This product provides a well-defined loss-of-function model for studying caveolin-2 (CAV2) biology without the use of monoclonal isolates, offering a broad representation of genetic edits that collectively abolish CAV2 expression. Researchers can employ these cells to dissect CAV2-dependent pathways in a robust and physiologically relevant epithelial cancer context.
The MES-OV cell line is an established human ovarian endometrioid carcinoma line, originally derived from a patient with ovarian cancer. These cells retain key epithelial characteristics and are widely used as a model system for investigating ovarian carcinogenesis, tumor progression, and drug response mechanisms. The line??s genetic stability and well-characterized signaling landscape make it particularly suitable for CRISPR-based engineering, enabling precise interrogation of gene function in pathways relevant to ovarian oncology.
CAV2 encodes caveolin-2, a critical structural component of caveolae that also functions in membrane trafficking, endocytosis, and signal transduction. CAV2 forms hetero-oligomeric complexes with caveolin-1 (CAV1) at the plasma membrane, where these invaginations compartmentalize signaling molecules. CAV2 participates in the regulation of EGFR internalization and downstream cascades such as the MAPK/ERK pathway (via ERK1/2) and the PI3K-AKT axis, impacting cell proliferation, survival, and migration. Disruption of CAV2 therefore perturbs caveolar integrity and signal compartmentalization, leading to attenuated responses to ligands like EGF and TGF-beta.
In the MES-OV ovarian cancer background, loss of CAV2 expression has significant consequences for oncogenic signaling. Given the reliance of many ovarian carcinomas on growth factor receptor trafficking and integrin-mediated adhesion, CAV2 knockout cells are expected to exhibit impaired caveolae-dependent EGFR internalization and reduced activation of downstream ERK1/2 and AKT. This results in diminished proliferative capacity, altered migratory behavior, and increased sensitivity to chemotherapeutic agents such as cisplatin and paclitaxel. The model thus serves as a powerful tool to dissect the contribution of caveolae to ovarian cancer malignancy and drug resistance.
These polyclonal knockout cells are suited for a wide range of downstream applications including Western blotting for CAV2, CAV1, EGFR, phospho-ERK, and phospho-AKT; immunofluorescence microscopy to assess caveolar architecture; flow cytometry for surface EGFR levels; MTT and BrdU proliferation assays; wound healing and Transwell migration/invasion studies; and co-immunoprecipitation of caveolin-protein complexes. Researchers can also use this model to evaluate drug sensitivity profiles in caveolin-deficient cancer cells. For detailed product information and technical assistance, please contact Ascent Research.
