This product consists of a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Ca Ski human cervical epidermoid carcinoma cell line, designed to disrupt the CD34 gene. The polyclonal format comprises a heterogeneous pool of edited cells harboring diverse gene disruptions, offering a robust and unbiased loss-of-function model that avoids clonal artifacts. This population enables comprehensive functional studies of CD34 in a cancer-relevant epithelial background, facilitating the assessment of gene disruption effects at the population level.
Ca Ski cells are an HPV16-positive epithelial cell line originally isolated from a cervical carcinoma metastasis, widely employed as a model for cervical cancer and human papillomavirus-associated malignancies. These cells retain key features of the original tumor, including anchorage-independent growth and invasive potential, making them suitable for investigating molecular mechanisms underlying cervical carcinogenesis. Their well-characterized genomic landscape and responsiveness to standard stimuli provide a reliable platform for gene editing and subsequent functional assays.
CD34 encodes a transmembrane sialomucin that functions as a cell surface adhesion molecule and signaling modulator. It interacts with L-selectin (CD62L) and integrins to mediate cell?Ccell and cell?Cmatrix adhesion, while also linking to intracellular signaling cascades through adaptors like CRKL. CD34 expression is transcriptionally regulated by hematopoietic transcription factors such as GATA2, RUNX1, and TAL1, and is induced by cytokines including G-CSF and GM-CSF. In turn, CD34 modulates downstream targets HOXB4, BMI1, and MYC, and participates in Notch and Wnt pathway regulation, with involvement of Notch1/RBP-J/HES1 and ??-catenin/LEF/TCF signaling modules. These interactions position CD34 at the nexus of adhesion-dependent signaling and stem cell maintenance programs.
Although CD34 is predominantly known as a hematopoietic stem cell marker, its aberrant expression has been reported in various solid tumors, including cervical carcinomas. In the Ca Ski polyclonal knockout model, disruption of CD34 permits investigation of its non-hematopoietic roles in epithelial cancer biology, such as modulation of cell adhesion, migration, and signal transduction. This model can reveal how loss of CD34 affects the invasive properties of cervical cancer cells and their response to extracellular cues, providing insights into CD34-dependent pathogenic mechanisms distinct from its classical hematopoietic functions.
This polyclonal knockout cell pool is well-suited for a range of functional analyses. Researchers can employ Transwell migration and invasion assays to quantify CD34-dependent motility, as well as cell adhesion assays to assess interactions with matrix or endothelial components. Gene expression profiling via RNA-seq or RT-qPCR can elucidate alterations in Notch and Wnt pathway components, while drug sensitivity profiling enables screening for CD34-related therapeutic vulnerabilities. Additional validation of CD34 loss can be performed by western blotting, flow cytometry, or immunofluorescence. For further details or to discuss customized applications, please contact Ascent Research.
