The DMD Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the MES-OV human ovarian carcinoma cell line. Engineered for targeted disruption of the DMD gene, this product serves as a loss-of-function model in which dystrophin protein expression is ablated. The polyclonal nature of the knockout pool retains the intrinsic genetic heterogeneity of the parental tumor line, providing a realistic cellular context for functional studies. Validated for absence of dystrophin, these cells are suitable for a wide range of downstream molecular and cellular analyses.
The MES-OV cell line is an immortalized human ovarian carcinoma model extensively utilized in cancer biology to investigate tumor progression, metastasis, and therapeutic resistance. Originating from patient tumor tissue, it recapitulates key phenotypic and molecular features of high-grade serous ovarian carcinoma, with robust adherent growth in vitro. This well-characterized background establishes a clinically relevant system for examining the role of dystrophin in epithelial malignancies, where its expression has been reported to be dysregulated and may contribute to altered cell adhesion and invasive capacity.
DMD encodes dystrophin, a cytoskeletal scaffold of the dystrophin?Cglycoprotein complex (DGC). It links actin to the extracellular matrix through ??-dystroglycan and sarcoglycans (??, ??, ??, ??), modulating adhesion, migration, and mechanotransduction. The DGC anchors syntrophins (SNTA1, SNTB1) and dystrobrevins (DTNA, DTNB), which regulate nNOS, MAPK/ERK, and PI3K/Akt signaling. DMD transcription is activated by MyoD, MEF2, and PAX3, and responsive to NF-??B and mechanical strain. CRISPR/Cas9-mediated disruption dismantles the DGC, severing cytoskeletal?Cmatrix linkages and altering downstream pathways.
In the context of MES-OV ovarian carcinoma, DMD knockout eliminates dystrophin-dependent cell?Cmatrix adhesion and likely compromises focal adhesion dynamics, which may affect migration and invasion??cellular behaviors central to peritoneal dissemination. This model enables dissection of dystrophin??s non-canonical functions outside skeletal muscle, providing insights into how the DGC intersects with oncogenic signaling networks. Given the observed upregulation of dystrophin in some carcinomas, the knockout system also allows investigation of dystrophin as a potential tumor suppressor or modulator of cancer progression.
These polyclonal knockout cells support analyses of cell adhesion, migration, and mechanotransduction via Boyden chamber, immunofluorescence, and adhesion assays. Western blot, qPCR, co-immunoprecipitation, and proteomic analyses verify DMD disruption and downstream signaling changes. The model also serves drug discovery for dystrophinopathies and studies of non-muscle dystrophinopathy manifestations. For batch-specific data, customization, or support, contact Ascent Research.
