IGF2BP3 Knockout Ca Ski Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal cell population derived from the HPV16-positive Ca Ski human cervical epidermoid carcinoma line, engineered for targeted disruption of the IGF2BP3 gene. This loss-of-function model enables systematic investigation of post-transcriptional gene regulatory mechanisms in a cervical cancer context. The polyclonal format preserves diverse editing outcomes across the population, offering a realistic cellular background for functional genomics studies.
Ca Ski is a well-established human cervical epidermoid carcinoma cell line that is positive for human papillomavirus type 16 (HPV16), a major etiological agent in cervical cancer. This adherent epithelial line retains key features of the original tumor, including expression of viral oncoproteins E6 and E7, and serves as a critical model for investigating HPV-driven oncogenesis, host-virus interactions, and therapeutic responsiveness.
IGF2BP3 encodes an oncofetal RNA-binding protein that post-transcriptionally regulates a network of pro-proliferative and pro-metastatic mRNAs by enhancing their stability and translation. It is transcriptionally activated by MYC and is responsive to Wnt and TGF-beta signaling cascades. IGF2BP3 forms ribonucleoprotein complexes with paralogs IGF2BP1 and IGF2BP2, as well as translation initiation factor eIF4E, nonsense-mediated decay factor UPF1, and poly(A)-binding protein PABPC1. Through these interactions, it stabilizes target transcripts such as MYC, CD44, CCND1, IGF2, and SNAI1 by shielding them from degradation and promoting their cap-dependent translation. Consequently, IGF2BP3 functions as a convergent node that integrates signals from PI3K/AKT, MAPK/ERK, Wnt/beta-catenin, and TGF-beta/SMAD pathways to drive cell proliferation, migration, and invasion.
In the Ca Ski cervical cancer context, disruption of IGF2BP3 is expected to attenuate cell proliferation, migration, and invasion by destabilizing key oncogenic and EMT-related mRNAs, thereby dampening downstream signaling through AKT, MAPK, and beta-catenin. This polyclonal knockout model permits functional dissection of IGF2BP3-dependent post-transcriptional regulatory modules and their contribution to cervical tumorigenesis. Moreover, the heterogeneous editing landscape mimics the genetic complexity of clinical tumors, enabling studies of how RNA-binding protein dysregulation influences cancer cell plasticity and metastatic dissemination. The model also facilitates investigation of potential functional redundancy among IGF2BP paralogs.
This IGF2BP3 knockout product is applicable in diverse research fields, including cancer biology, RNA biology, and metastasis. Standard characterization involves Western blotting to confirm protein loss and RT-qPCR to assess target transcript levels; broader transcriptomic effects can be delineated by RNA-seq. Protein?CRNA interactions are dissected using RNA immunoprecipitation, while functional consequences are measured in proliferation, migration, and invasion assays. The polyclonal nature makes it suited for drug target validation and for screening chemical inhibitors of RNA-binding protein function. Additionally, the model supports exploration of post-transcriptional regulatory networks in HPV-driven cancers and can be combined with ectopic expression or rescue experiments to verify phenotype specificity. For further technical details or to discuss custom applications, please contact Ascent Research.
