CD34 Knockout A2780 Polyclonal Cells are a population of human A2780 ovarian carcinoma epithelial cells with CRISPR/Cas9-mediated disruption of the CD34 gene. This polyclonal product, derived from the endometrioid adenocarcinoma A2780 cell line, provides a heterogeneous loss-of-function model for investigating CD34-dependent processes without prior clone isolation.
The A2780 cell line is a widely used model of ovarian cancer, offering a relevant epithelial background to study tumorigenesis, metastasis, and drug resistance. Integrating a CD34 knockout into this system allows focused interrogation of CD34??s contributions to cell adhesion, migration, and stem cell-like phenotypes in an oncogenic context.
CD34 encodes a transmembrane sialomucin that serves as a cell adhesion molecule and a marker of hematopoietic progenitors and endothelial cells. Its expression is regulated by VEGF and Notch signaling, as well as transcription factors GATA-2, RUNX1, and ETS. CD34 interacts with L-selectin and E-selectin to promote cell adhesion, and signals through PI3K/Akt, MAPK/ERK, and focal adhesion kinase (FAK) pathways. Interacting partners CRKL and LMO2 further link CD34 to cytoskeletal dynamics and transcriptional control. Disrupting CD34 thus impairs adhesion cascades and downstream signaling, altering cellular behavior.
In ovarian cancer, CD34 knockout offers a model to dissect tumor?Cmicroenvironment interactions. Loss of CD34-mediated adhesion may affect peritoneal dissemination and angiogenesis, while potential effects on cancer stem cell properties enable investigation of self-renewal and differentiation. This model helps evaluate how CD34 loss modifies invasive and metastatic potential in A2780 cells.
Applications include cancer stem cell and tumor microenvironment studies, drug target validation, and functional assays such as migration, invasion, adhesion, colony formation, and drug sensitivity testing. Flow cytometry and western blotting can confirm CD34 knockout and downstream signaling changes. Hematopoietic lineage studies may also utilize this model when CD34 is ectopically expressed. For further inquiries, contact Ascent Research.
