The EFEMP1 Knockout MES-OV Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human ovarian cancer cell line MES-OV. This product provides targeted disruption of the EFEMP1 gene, encoding fibulin-3, an extracellular matrix glycoprotein. The polyclonal format offers a heterogeneous pool of knockout cells, capturing diverse editing events without clonal selection. This loss-of-function model is designed for investigating fibulin-3??s roles in ovarian cancer, particularly cell adhesion, migration, and matrix remodeling, and is suitable for various in vitro assays.
The MES-OV cell line, derived from a human ovarian adenocarcinoma, is a well-established model for ovarian cancer research. It retains characteristic features such as aberrant adhesion, invasive potential, and altered responses to extracellular matrix cues. Importantly, MES-OV cells endogenously express fibulin-3, providing a physiologically relevant background for functional studies. In ovarian cancer, fibulin-3-mediated matrix interactions can influence tumor progression and therapeutic resistance, making this cell line an ideal host for dissecting EFEMP1??s roles.
EFEMP1 encodes fibulin-3, an ECM glycoprotein involved in cell adhesion and matrix organization. It interacts with integrins (e.g., ??V??3) and binds collagen, fibronectin, heparan sulfate proteoglycans, and TIMP-3. These interactions link to focal adhesion kinase (FAK) and Src, activating PI3K/Akt/mTOR pathways. EFEMP1 is regulated by TGF-??, EGF, and miR-29, and downstream it modulates MMPs and TIMPs, impacting matrix turnover. Additionally, fibulin-3 influences caspases, suggesting roles in apoptosis. Through these networks, EFEMP1 coordinates adhesion and survival signaling.
Knockout of EFEMP1 in MES-OV cells is expected to impair integrin-mediated adhesion and reduce ECM-derived survival signals. Loss of fibulin-3 may decrease FAK phosphorylation and PI3K/Akt activity, sensitizing cells to anoikis. Altered MMP activity can further affect matrix remodeling and invasion. In ovarian adenocarcinoma, this may disrupt the balance between survival and death, and modify the tumor microenvironment. This model thus aids in studying ECM dependence and drug resistance mechanisms, particularly against the PI3K/Akt pathway.
This polyclonal knockout population supports diverse functional assays, including cell adhesion, migration/invasion, Western blotting for phospho-Akt and FAK, immunofluorescence of focal adhesions, anoikis assays, and drug sensitivity testing. Transcriptomic analysis via RNA-seq and flow cytometry for apoptosis further expand applications. The model enables investigation of ECM-mediated drug resistance, tumor microenvironment interactions, and synthetic lethality. For further information, please contact Ascent Research.
