The CD109 Knockout 786-O Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout population that disrupts the CD109 gene in the human clear cell renal carcinoma cell line 786-O. This polyclonal model, generated through guide RNA-directed Cas9 nuclease activity, introduces heterogeneous loss-of-function mutations across the targeted locus. The resulting cell population enables robust and reproducible investigation of CD109-dependent phenotypes without the constraints of single-cell clone selection. As a polyclonal resource, it maintains genetic diversity typical of the original cell line while collectively abrogating CD109 protein expression, making it well-suited for pooled functional assays and high-throughput screening applications in cancer biology.
Derived from a primary clear cell renal cell carcinoma, 786-O is an adherent epithelial cell line widely used as an in vitro model for kidney cancer research. This line harbors hallmark molecular features of renal carcinoma, including VHL inactivation, and faithfully recapitulates aspects of tumor cell signaling and metabolism. Its well-characterized background provides a physiologically relevant context for exploring the contribution of CD109 to renal tumorigenesis. The 786-O platform supports diverse experimental endpoints, from biochemical pathway dissection to phenotypic analyses of cell motility and adhesion, offering a dependable host for interrogating gene function in clear cell renal carcinoma.
CD109 encodes a GPI-anchored cell surface glycoprotein that serves as a co-receptor and negative regulator of TGF-?? signaling. Mechanistically, CD109 binds to TGF-?? receptor I (T??RI) and TGF-?? receptor II (T??RII), inhibiting phosphorylation of the downstream effectors SMAD2 and SMAD3. This suppression blunts their association with SMAD4 and subsequent transcriptional activation of target genes such as PAI-1 and CTGF. Beyond TGF-??, CD109 engages integrin-??1 and CD44 to modulate cell adhesion and migration, and it influences JAK/STAT signaling through effects on STAT3 activation. Upstream regulators including TGF-??1, EGF, IL-1??, and TNF-?? can tune CD109 expression, while downstream impacts extend to focal adhesion kinase (FAK) and Src kinase networks, linking CD109 to ECM-receptor interaction pathways.
In the 786-O background, disruption of CD109 removes a critical brake on TGF-??/SMAD signaling, leading to enhanced SMAD2/3 phosphorylation and upregulated expression of TGF-??-responsive genes. This dysregulation can alter integrin-mediated adhesion and migratory behavior, potentially shifting the balance from a tumor-suppressive to a pro-invasive phenotype. The knockout model therefore enables precise dissection of CD109??s dual roles in renal carcinoma, allowing researchers to determine whether loss of CD109 promotes or suppresses tumorigenic traits in a clear cell renal carcinoma context. By comparing the polyclonal knockout population to parental 786-O cells, investigators can delineate CD109-dependent effects on signal transduction, cell dynamics, and drug sensitivity.
This CD109 knockout cell model is designed for a broad range of biomedical research applications, including mechanistic studies of TGF-??/SMAD pathway modulation, functional analyses of cell adhesion and migration, and exploration of CD109 as a modulator of therapeutic response. Representative assays range from Western blotting for phospho-SMAD2/3 and RT-qPCR for PAI-1 or CTGF transcript levels to cell invasion, adhesion, and transcriptomic profiling via RNA-seq. The polyclonal format is particularly suited for pooled functional genomic screens and dose-response studies where a diverse allelic background reflects natural tumor heterogeneity. For further technical details and ordering information, please contact Ascent Research.
