The JUN Knockout Ca Ski Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Ca Ski human cervical carcinoma cell line. This product features targeted disruption of the JUN gene, eliminating functional c-Jun protein. The polyclonal format provides a heterogeneous pool of knockout cells, avoiding clonal selection artifacts and enabling robust population-level analyses of JUN-dependent signaling networks.
The host Ca Ski cell line originates from a metastatic lesion in the small intestine of a cervical epidermoid carcinoma patient. It is HPV16-positive and constitutively expresses the viral oncoproteins E6 and E7, which inactivate p53 and retinoblastoma tumor suppressors. Ca Ski cells retain an epithelial morphology and are widely used as a model for HPV-driven cervical carcinogenesis, tumor biology, and therapeutic screening. Their stable genomic background ensures reliable gene-editing outcomes.
JUN encodes a basic leucine zipper (bZIP) transcription factor that forms the core of the activator protein-1 (AP-1) complex. It dimerizes with other AP-1 members??such as c-Fos, FosB, Fra-1, Fra-2, ATF2, and NFAT??to regulate gene expression. JUN is activated by MAPK cascades: ERK, JNK, and p38, downstream of growth factors (EGF, PDGF) and pro-inflammatory cytokines (TNF-??, IL-1). Phosphorylated JUN transcriptionally controls targets including cyclin D1 (cell cycle), Bcl-2 (apoptosis), MMP-9 (invasion), VEGF (angiogenesis), and p53 (stress response). JUN also interacts with coactivators p300/CBP and integrates signals from Wnt/??-catenin/TCF-LEF and TGF-??/Smad3 pathways.
In cervical cancer, HPV E6/E7 oncoproteins aberrantly upregulate AP-1 activity, making JUN a critical driver of malignant phenotypes such as uncontrolled proliferation, apoptosis evasion, epithelial-to-mesenchymal transition (EMT), and invasion. The Ca Ski polyclonal JUN knockout model therefore provides a physiologically relevant platform to dissect HPV-JUN oncogenic cooperation and assess the consequences of JUN loss in an HPV-positive context. It is particularly valuable for studying how JUN influences downstream effectors like p53 and ATF2 and for revealing compensatory mechanisms.
This knockout cell population supports a broad range of applications, including western blotting for total and phospho-JUN, RT-qPCR profiling of JUN target genes, ChIP-qPCR for AP-1 binding, luciferase reporter assays, proliferation (MTT/BrdU) and apoptosis (annexin V) assays, and migration/invasion studies. Co-immunoprecipitation experiments allow examination of JUN-containing complexes, and RNA-seq enables transcriptomic comparisons between wild-type and knockout states. The model is also suitable for drug sensitivity screens to identify AP-1-dependent therapeutic vulnerabilities. For further information, technical support, or to request a quote, please contact Ascent Research.
