The IGF2BP3 Knockout KYSE-150 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the KYSE-150 human esophageal squamous cell carcinoma line. This product features targeted disruption of the IGF2BP3 gene, which encodes an oncofetal RNA-binding protein implicated in post-transcriptional regulation of numerous oncogenic transcripts. The polyclonal format provides a heterogeneous pool of edited cells, enabling robust loss-of-function studies without the potential biases of single-cell clonal selection. It is supplied as a ready-to-use population of viable, proliferating cells, suitable for immediate expansion and experimental deployment.
The KYSE-150 host cell line is a widely used model of poorly differentiated esophageal squamous cell carcinoma (ESCC). It exhibits adherent epithelial morphology and carries a mutation in the TP53 tumor suppressor gene, reflecting the genetic instability commonly observed in ESCC. This cell line retains key oncogenic features of esophageal cancer, including dysregulated proliferation and invasive potential, making it particularly valuable for investigating molecular drivers of ESCC malignancy and therapeutic resistance.
IGF2BP3 functions as an mRNA-binding protein that recognizes N6-methyladenosine (m6A)-modified transcripts and enhances their stability and translational efficiency. It is transcriptionally activated by MYC and the ??-catenin/TCF complex, as well as by hypoxia-induced HIF-1?? and inflammatory NF-??B signaling, while being negatively regulated by the let-7 family of microRNAs. Major downstream targets include MYC, CD44, CDK6, BMI1, HMGA2, LIN28B, and SNAI1. Through stabilization of these mRNAs, IGF2BP3 promotes cell cycle progression, stemness maintenance, and epithelial-mesenchymal transition (EMT). The protein interacts with other IGF2BP family members, HNRNPU, and polysomal complexes to orchestrate oncogenic mRNA networks, positioning it as a central node in PI3K/AKT, MAPK/ERK, and Wnt/??-catenin cascades.
In the context of KYSE-150 ESCC cells, IGF2BP3 overexpression is associated with enhanced proliferation, migration, and invasion, mirroring its clinical correlation with poor prognosis in esophageal cancer patients. Disruption of IGF2BP3 in this p53-mutant background is expected to reduce the stability and translation of key target mRNAs, thereby attenuating the aggressive phenotype. This knockout model thus provides a physiologically relevant system to dissect the post-transcriptional layer of oncogenic signaling in ESCC and to evaluate the therapeutic potential of targeting RNA-binding proteins.
This polyclonal knockout cell pool is ideally suited for a range of functional assays, including Western blotting and RT-qPCR to confirm depletion of IGF2BP3 and altered expression of downstream targets, RNA immunoprecipitation (RIP) to study m6A-dependent interactions, and phenotypic assays such as MTT, colony formation, Transwell migration/invasion, and Annexin V apoptosis analysis. It also enables transcriptome-wide studies via RNA-seq and in vivo xenograft models to assess tumorigenicity. For further technical specifications or to discuss custom services, please contact Ascent Research.
