The CD44 Knockout MES-OV Polyclonal Cells represent a CRISPR/Cas9-engineered ovarian cancer model in which the CD44 gene has been disrupted across a heterogeneous cell population. This polyclonal knockout product, generated from the MES-OV human ovarian adenocarcinoma cell line, provides a loss-of-function tool for investigating CD44-dependent processes without the clonal selection artifacts associated with single-cell-derived lines. The use of CRISPR/Cas9-mediated gene disruption ensures robust abrogation of CD44 expression, enabling researchers to dissect its role in cancer biology with high biological relevance.
The MES-OV cell line, established from a patient with epithelial ovarian carcinoma, retains key features of high-grade serous ovarian cancer, including genomic instability and aggressive growth characteristics. This cell line is widely employed in ovarian cancer research to study tumor progression, metastasis, and drug resistance. By leveraging this clinically relevant background, the CD44 knockout polyclonal cells offer a physiologically appropriate system to examine the molecular underpinnings of ovarian cancer malignancy.
CD44 is a multifunctional transmembrane receptor for hyaluronic acid (HA) and other ligands, including osteopontin and matrix metalloproteinases. Upon ligand engagement, CD44 recruits ERM proteins (ezrin, radixin, moesin) and activates downstream effectors such as RhoA/Rac1 GTPases, PI3K/Akt, and MAPK/ERK pathways. These cascades transduce signals to transcription factors like NF-??B, AP-1, and ??-catenin/TCF-LEF, driving the expression of genes involved in cell proliferation (Cyclin D1), matrix remodeling (MMP9), and epithelial-mesenchymal transition (EMT). CD44 also interacts with growth factor receptors (EGFR, c-Met) and integrins, integrating adhesion and signaling. Upstream regulators include TGF-??, EGF, and Wnt ligands, positioning CD44 at a nexus of oncogenic pathways.
In the context of ovarian cancer, CD44 is frequently associated with tumor-initiating cells, metastatic propensity, and chemoresistance. Its overexpression in MES-OV cells has been linked to enhanced migration, invasion, and stem cell-like phenotypes. Disrupting CD44 in this polyclonal model disrupts HA-mediated adhesion and attenuates key signaling networks, leading to reduced invasive capacity and diminished sphere-forming ability. Thus, these knockout cells serve as a powerful platform for elucidating CD44??s contribution to ovarian cancer progression and for identifying downstream vulnerabilities.
Typical applications include studying tumor cell migration and invasion using Transwell assays, evaluating cancer stem cell properties via sphere formation, and assessing signaling pathway alterations through western blotting or RT-qPCR. The model is also suited for investigating drug resistance mechanisms and for xenograft tumorigenicity studies to assess metastatic potential in vivo. Additional assays such as flow cytometry for CD44 surface expression, HA binding assays, and apoptosis analyses further expand the utility of these polyclonal knockout cells. For technical specifications, pricing, or to request a quote, please contact Ascent Research.
