The EHBP1 Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited heterogeneous population derived from the MES-OV human ovarian cancer cell line, featuring disruption of the EHBP1 gene via a pool of guide RNAs. This polyclonal knockout format provides a model system that captures a spectrum of loss-of-function mutations, reducing clonal bias and better reflecting the genetic diversity of tumor cell populations. Such a product is well-suited for pooled screening applications and studies where physiological gene inactivation is critical.
MES-OV is a well-established model of ovarian carcinoma, exhibiting epithelial morphology and tumorigenic behavior. These cells display characteristic markers of high-grade serous ovarian cancer and serve as a reliable platform for exploring oncogenic signaling and drug responses. Their invasive and migratory properties make them particularly valuable for studying processes relevant to ovarian cancer metastasis and intratumoral heterogeneity.
EHBP1 functions as an adaptor scaffold linking EH domain-containing proteins EHD1 and EHD2 to the endocytic recycling pathway and the actin cytoskeleton. Upon BDNF stimulation, EHBP1 interacts with clathrin-coated vesicle components and Rab GTPases to facilitate recycling of TrkB receptors to the plasma membrane. This cycle is activated by growth factors and receptor tyrosine kinases and is essential for maintaining surface receptor levels and downstream signaling; knockout of EHBP1 impairs TrkB surface expression and disrupts EHD-mediated endocytic trafficking.
In the ovarian cancer context, loss of EHBP1 is expected to perturb the recycling of receptors that drive cell proliferation, migration, and invasion. By attenuating BDNF?CTrkB signaling and disrupting actin cytoskeleton remodeling, EHBP1 knockout may reduce the tumorigenic and metastatic capacity of MES-OV cells. This model thus provides a powerful tool to investigate how endocytic trafficking dysregulation contributes to ovarian cancer progression and may identify vulnerabilities related to receptor recycling.
Applications include quantitative assays of transferrin recycling, immunofluorescence for endosomal markers like EEA1 and Rab11, and phospho-TrkB analysis to measure signaling alterations. Migration and invasion assays combined with transcriptomic profiling can map the full impact of EHBP1 loss on cell behavior. These polyclonal knockout cells are an invaluable resource for studies of receptor trafficking in cancer. For further information, contact Ascent Research.
