The IGF2BP3 Knockout CAL-27 Polyclonal Cells represent a CRISPR/Cas9-mediated polyclonal knockout population derived from the human tongue squamous cell carcinoma cell line CAL-27. This product is generated through targeted gene disruption of the IGF2BP3 locus, resulting in a heterogeneous pool of cells carrying loss-of-function mutations in the IGF2BP3 gene. As a polyclonal knockout resource, it provides a robust model for examining the functional consequences of IGF2BP3 ablation without the clonal bias inherent in monoclonal lines, enabling large-scale screening and pooled functional assays.
CAL-27 is an adherent epithelial cell line isolated from a human tongue squamous cell carcinoma, a prevalent form of oral squamous cell carcinoma (OSCC). These cells exhibit classic epithelial morphology and retain key oncogenic properties, including constitutive activation of growth signaling cascades and migratory capability. CAL-27 serves as a well-characterized in vitro model for oral cancer, widely employed in studies of tumorigenesis, drug response, and metastasis, rendering it an ideal host for investigating RNA-binding protein function in this cancer type.
IGF2BP3 (insulin-like growth factor 2 mRNA-binding protein 3) is an oncofetal RNA-binding protein that post-transcriptionally regulates the stability and translation of a cohort of pro-proliferative and pro-metastatic mRNAs. It directly binds and stabilizes MYC, CD44, CDK6, SNAI1, and BCL2 transcripts, thereby enhancing their protein expression. IGF2BP3 activity is modulated by upstream regulators including the MYC transcription factor, growth factor stimuli such as IGF-1 and EGF, and the let-7 microRNA. Within the signaling network, IGF2BP3 functions downstream of PI3K/AKT/mTOR and MAPK/ERK cascades, and intersects with WNT/??-catenin signaling to promote epithelial-mesenchymal transition (EMT) via SNAI1. The protein forms complexes with translation initiation factor eIF4E, the DROSHA microprocessor, and stress granule components, facilitating efficient translation of oncogenic transcripts. Knockout of IGF2BP3 in CAL-27 cells disrupts this post-transcriptional regulatory hub, leading to diminished expression of key oncogenic drivers and attenuation of aggressive cancer phenotypes.
In the context of CAL-27 oral cancer cells, loss of IGF2BP3 impairs the stabilization and translational enhancement of MYC and CD44 mRNAs, resulting in reduced proliferation, migration, and invasion. This polyclonal knockout population thereby captures a range of loss-of-function effects arising from heterogeneous gene disruptions, faithfully modeling the variability of IGF2BP3 inactivation. Consequently, it serves as a valuable system for dissecting the role of post-transcriptional gene regulation in OSCC progression and for defining the contribution of IGF2BP3 to EMT and metastatic dissemination.
This IGF2BP3 Knockout CAL-27 Polyclonal Cells product is suited for diverse research applications, including functional genomics of RNA-binding proteins in cancer, oral cancer disease modeling, drug target validation, metastasis mechanism studies, and therapeutic screening. Researchers can employ a variety of downstream assays such as western blotting to confirm IGF2BP3 and target protein ablation, RT-qPCR to assess target mRNA levels, RNA sequencing for transcriptome-wide profiling, cell proliferation assays (e.g., MTT), Transwell migration and invasion assays, Annexin V?based apoptosis detection, and drug sensitivity testing against candidate therapeutics. For additional information or technical support, please contact Ascent Research.
