The CD109 Knockout A2780 Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal knockout cell population engineered to disrupt the CD109 gene in the A2780 human ovarian cancer cell line. This loss-of-function model provides a genetically heterogeneous pool of cells with CD109 gene disruption, enabling robust functional studies without clonal selection biases. The polyclonal format is well-suited for population-level analyses of TGF-?? signaling and ovarian cancer biology, offering a versatile research tool for dissecting CD109-mediated pathways.
The parental A2780 cell line was derived from an untreated ovarian carcinoma patient and exhibits epithelial morphology characteristic of ovarian adenocarcinoma. Widely employed as a model for ovarian cancer, these cells retain key features of the disease, including responsiveness to cytokines and growth factors relevant to tumor progression. The A2780 background provides a clinically pertinent platform for investigating molecular mechanisms underlying ovarian tumorigenesis, metastasis, and therapeutic resistance.
CD109 is a glycosylphosphatidylinositol (GPI)-anchored surface antigen that functions as a negative regulator of TGF-?? signaling. Mechanistically, CD109 acts as a co-receptor for transforming growth factor-beta (TGF-??), facilitating the internalization and degradation of TGF-?? receptor complexes (TGFBR1/TGFBR2), thereby attenuating downstream SMAD2/3 activation. This regulatory axis intersects with other signaling cascades mediated by epidermal growth factor (EGF) and interleukins, and influences downstream effectors including STAT3, Akt, and matrix metalloproteinases (MMPs). CD109 also interacts with integrins, linking TGF-?? signaling to cell adhesion and migration. Perturbation of CD109 expression is known to modulate epithelial-mesenchymal transition (EMT) programs, making it a critical node in cancer cell plasticity.
In the A2780 ovarian adenocarcinoma context, knockout of CD109 is expected to enhance TGF-??-driven signaling, potentially promoting EMT and associated changes in cellular motility and invasion. This model enables dissection of CD109??s role in maintaining epithelial integrity and suppressing tumor aggressiveness. Given the involvement of TGF-?? in tumor microenvironment interactions and drug resistance, the CD109 knockout cells serve as a pertinent system for exploring how loss of this surface antigen reconfigures signal transduction networks and influences ovarian cancer pathophysiology.
The CD109 Knockout A2780 polyclonal cells are suitable for a variety of applications, including western blotting for phosphorylated SMAD2/3, RT-qPCR for TGF-?? target genes, migration and invasion assays, immunofluorescence for E-cadherin and vimentin, flow cytometry for surface CD109, and co-immunoprecipitation of TGF-?? receptors. Drug sensitivity studies with TGF-?? inhibitors or chemotherapeutics further augment the model’s utility. For additional information, please contact Ascent Research.
