The CCM2 Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human ovarian carcinoma MES-OV cell line. This product introduces a loss-of-function disruption in the CCM2 gene, enabling studies of CCM2-dependent signaling and cellular processes. The polyclonal format reflects a heterogeneous pool of edited cells, suitable for functional assays that do not require clonal isolation.
The MES-OV cell line is an established model of human ovarian adenocarcinoma with a pronounced mesenchymal phenotype, exhibiting tumorigenic properties and the capacity for invasion and metastasis. These cells display epithelial-mesenchymal plasticity, making them a relevant platform for investigating pathways that regulate cell migration, adhesion, and vascular interaction in cancer biology.
CCM2 encodes a scaffold protein that is a core component of the CCM complex. It negatively regulates MAPK/ERK and RhoA/ROCK signaling downstream of integrin engagement, interacting with CCM1/KRIT1, CCM3/PDCD10, ICAP1, and MEKK3. Loss of CCM2 disrupts this regulation, leading to increased ERK1/2 phosphorylation, elevated RhoA/ROCK activity, destabilization of VE-cadherin, and altered expression of KLF2 and KLF4.
In the context of MES-OV cells, disruption of CCM2 is particularly informative due to their mesenchymal characteristics and invasive potential. The CCM signaling axis intersects with integrin-mediated adhesion and cytoskeletal reorganization, pathways that are frequently dysregulated during ovarian carcinoma progression. By eliminating CCM2 function, researchers can examine how loss of CCM complex integrity influences cell migration, Rho GTPase dynamics, and MAPK/ERK activation, thereby modeling aspects of cancer metastasis and vascular malformation in a tumor-relevant setting.
This knockout model supports a range of research applications, including the study of CCM signaling in tumor cell motility, dissection of integrin-dependent pathways, and screening of therapeutics targeting CCM2-related mechanisms. Typical assays applicable include western blotting for ERK1/2 phosphorylation, RT-qPCR for KLF2 and KLF4, immunofluorescence for VE-cadherin, Rho GTPase activation assays, transwell migration and wound healing assays, and cell adhesion assays. These polyclonal knockout cells provide a versatile tool for investigating vascular malformations and cancer metastasis. For further technical inquiries, please contact Ascent Research.
