The EHBP1L1 Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the human MES-OV ovarian serous cystadenocarcinoma cell line, offering a loss-of-function model for the EHBP1L1 gene. This polyclonal pool contains diverse editing events across the population, avoiding clonal biases and providing a robust tool for population-level functional studies without the need for single-cell cloning. The cells are supplied as a ready-to-use format for investigating EHBP1L1-dependent mechanisms in an ovarian cancer context.
The MES-OV cell line originates from a malignant effusion of an ovarian serous cystadenocarcinoma patient and maintains an epithelial-like morphology. It recapitulates key molecular features of high-grade serous ovarian carcinoma, making it an established model for studying ovarian cancer biology, metastatic progression, and therapeutic responses. Its well-characterized genetic background supports credible functional genomics and drug discovery research.
EHBP1L1 functions as a scaffold linking Rho GTPase signaling to endocytic actin dynamics, thereby regulating cell polarity and migration. It acts downstream of Cdc42 and Rac1, with input from PI3K/Akt, and interacts directly with Rab8, Rab11, Eps15 homology domain proteins, and the Arp2/3 complex. Through these interactions, EHBP1L1 coordinates Rab-dependent membrane trafficking and cytoskeletal reorganization, influencing actin polymerization, endocytic vesicle recycling, and cell adhesion molecule distribution. Its disruption impacts processes central to carcinoma metastasis.
In MES-OV ovarian cancer cells, EHBP1L1 knockout enables dissection of its role in invasion and polarity, which are critical for metastatic dissemination. Loss of EHBP1L1 may impair endocytic trafficking of receptors involved in proliferation and migration, and alter actin dynamics, potentially reducing tumor cell motility. This model is thus highly relevant for probing EHBP1L1 contributions to ovarian cancer metastasis and for evaluating targeted therapeutic strategies.
Researchers can utilize this polyclonal knockout model for functional assays including wound-healing and transwell invasion assays, immunofluorescence analysis of actin and vesicle markers, and co-immunoprecipitation to map EHBP1L1 interaction networks. Downstream molecular characterization may involve Western blotting, RT-qPCR, and phospho-signaling profiling of Cdc42/Rac1/Akt pathways. Drug sensitivity testing can also be performed to assess EHBP1L1 loss on chemotherapeutic efficacy. For more information or to place an order, please contact Ascent Research.
