The EFHD1 Knockout MES-OV Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population generated by disrupting the EFHD1 gene in the MES-OV human ovarian cancer cell line. This heterogeneous pool of edited cells carries diverse loss-of-function mutations, providing a robust model for investigating EFHD1??s cellular roles without the artifacts of clonal selection. The polyclonal format preserves population-level heterogeneity, enhancing physiological relevance for functional studies.
MES-OV is a well-characterized human ovarian adenocarcinoma cell line that serves as a model for ovarian cancer biology. Derived from a patient tumor, these cells exhibit key malignant features including uncontrolled proliferation, migratory capacity, and invasive potential. As a representative epithelial ovarian cancer model, MES-OV is particularly suited for examining genes involved in tumor progression and metastasis, making it an appropriate host for EFHD1 knockout.
EFHD1 is a calcium-binding protein that links cytosolic Ca2+ signals to mitochondrial apoptosis and actin cytoskeleton remodeling. Upon calcium stimulation, EFHD1 translocates to mitochondria and interacts with BAX, VDAC, and Cyclophilin D, promoting BAX-mediated cytochrome c release and caspase-9/-3 activation to execute intrinsic apoptosis. EFHD1 also binds actin and cofilin to regulate filament dynamics and cell migration. Transcriptionally regulated by TP53, EFHD1 integrates apoptotic stimuli with calcium homeostasis, and influences mitochondrial fragmentation through DRP1, positioning it at the intersection of cell death and motility pathways.
In ovarian cancer, EFHD1??s dual function in apoptosis and migration is critical; its loss may impair apoptotic pathways, contributing to chemoresistance, while perturbing actin-driven motility could alter metastatic behavior. Knocking out EFHD1 in MES-OV cells enables dissection of how calcium-dependent mitochondrial signaling and cytoskeletal reorganization impact tumor cell survival, invasion, and drug response, providing insights into mechanisms driving ovarian cancer malignancy.
This knockout model supports diverse applications, including apoptosis analysis by flow cytometry and Western blotting, migration and invasion assays, mitochondrial membrane potential measurements, and co-immunoprecipitation of EFHD1 interactors like BAX and actin. It is also suitable for drug sensitivity testing and high-content immunofluorescence studies of mitochondrial morphology and actin organization. For more information, contact Ascent Research.
