The CCM2 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the A2780 human ovarian carcinoma cell line, featuring targeted disruption of the CCM2 gene. This polyclonal knockout model provides a heterogeneous loss-of-function system for studying CCM2-dependent processes without clonal selection artifacts.
A2780 cells are an epithelial ovarian cancer cell line originally established from an untreated patient, widely used in ovarian cancer research and tumor microenvironment studies. These cells retain key signaling pathways relevant to angiogenesis, migration, and cell-cell junction regulation, making them a suitable platform for investigating CCM2 function in a cancer context.
CCM2 encodes a scaffold protein that forms the core of the CCM complex together with KRIT1 and PDCD10. This complex operates downstream of integrins, VEGF, and angiopoietin-1/TIE2 signaling to maintain endothelial barrier integrity. Mechanistically, CCM2 negatively regulates RhoA/ROCK signaling and positively couples to MEKK3-p38 MAPK cascades, thereby controlling transcription factors such as KLF2 and KLF4. Loss of CCM2 leads to RhoA activation, MLCK-mediated stress fiber formation, and increased vascular permeability, while also perturbing MAPK-dependent gene expression programs.
In the A2780 background, CCM2 disruption allows investigation of how ovarian cancer cells modulate junctional properties, contractility, and paracrine signaling within the tumor microenvironment. Although CCM2 is primarily studied in endothelial cells, its expression and potential roles in epithelial cancer cells make this model valuable for dissecting tumor cell?Cendothelial communication, angiogenesis, and metastasis. The A2780 line??s well-characterized signaling responses to VEGF and angiopoietin-1 further enable precise study of CCM2??s position in these pathways.
This polyclonal knockout cell population is suitable for a range of functional assays, including western blotting to confirm CCM2 loss, RhoA activation assays, immunofluorescence for junction proteins, and transwell permeability or migration/invasion assays. It can be employed to model cerebral cavernous malformation?Clike signaling defects in a cancer setting, explore tumor angiogenesis mechanisms, or evaluate therapeutic interventions targeting the RhoA/ROCK or MAPK axes. For additional information or technical support, please contact Ascent Research.
